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ChIP Cross-link Gold

目录号

格式

价格

C01019027

600 µl

$150.00

Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. However, formaldehyde is usually not effective in cross-linking proteins that are not directly bound to the DNA. For example, inducible transcription factors or cofactors interact with DNA through protein-protein interactions, and these are not well preserved with formaldehyde. For such higher order and/or dynamic interactions such as this, other cross-linkers should be considered for efficient protein-protein stabilization. Diagenode's ChIP cross-link Gold which is used in combination with formaldehyde is an excellent choice for such higher order protein interactions.

方案
Chromatin shearing - Guide for successful chromatin preparation using the Bioruptor^® Pico
Chromatin immunoprecipitation (ChIP) is a common tool used to study protein-DNA interactions in c... Download
文档
ChIP cross-link Gold MANUAL
The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linkin... Download

出版物

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Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO
Camera F. et al.
Iroquois transcription factor gene IRX3 is highly expressed in 20â€“30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences âˆ¼220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with th...

Targeting lymphoid-derived IL-17 signaling to delay skin aging.
Paloma S. et al.
Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-...

Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.
Tzeplaeff L. et al.
Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalizati...

Smc5/6 silences episomal transcription by a three-step function.
Abdul F. et al.
In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a t...

Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.
Schomann T. et al.
The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (A...

Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer
Schenk MW et al.
Small cell lung cancer (SCLC) has a 5-year survival rate of \<7\%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patien...

Regulatory interplay between Vav1, Syk and β-catenin occurs in lungcancer cells.
Boudria Rofia et al.
Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. ...

Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.
Ryan, Genevieve E. et al.
Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens ...

BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma
Laubscher et. al.
Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters...

The Human Integrator Complex Facilitates Transcriptional Elongation by Endonucleolytic Cleavage of Nascent Transcripts.
Beckedorff F, Blumenthal E, daSilva LF, Aoi Y, Cingaram PR, Yue J, Zhang A, Dokaneheifard S, Valencia MG, Gaidosh G, Shilatifard A, Shiekhattar R
Transcription by RNA polymerase II (RNAPII) is pervasive in the human genome. However, the mechanisms controlling transcription at promoters and enhancers remain enigmatic. Here, we demonstrate that Integrator subunit 11 (INTS11), the catalytic subunit of the Integrator complex, regulates transcription at these loci...

Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming.
Suryo Rahmanto Y, Shen W, Shi X, Chen X, Yu Y, Yu ZC, Miyamoto T, Lee MH, Singh V, Asaka R, Shimberg G, Vitolo MI, Martin SS, Wirtz D, Drapkin R, Xuan J, Wang TL, Shih IM
Somatic inactivating mutations of ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human endometrium-related malignancies. To elucidate the mechanisms underlying how ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murine models with Arid1a and/or Pten c...

AP-1 controls the p11-dependent antidepressant response.
Chottekalapanda RU, Kalik S, Gresack J, Ayala A, Gao M, Wang W, Meller S, Aly A, Schaefer A, Greengard P
Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations ...

A stress-responsive enhancer induces dynamic drug resistance in acute myeloid leukemia.
Williams MS, Amaral FM, Simeoni F, Somervaille TC
The drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts for treatment failure in acute myeloid leukemia (AML). In this study, we identified and functionally validated the network of enhancers that controls expression of ABCB1. We show that exposure of leukemia cells to daunorubici...

The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress.
Moreno Leon L, Gautier M, Allan R, Ilié M, Nottet N, Pons N, Paquet A, Lebrigand K, Truchi M, Fassy J, Magnone V, Kinnebrew G, Radovich M, Cheok MH, Barbry P, Vassaux G, Marquette CH, Ponzio G, Ivan M, Pottier N, Hofman P, Mari B, Rezzonico R
Lung cancer is the leading cause of cancer death worldwide, with poor prognosis and a high rate of recurrence despite early surgical removal. Hypoxic regions within tumors represent sources of aggressiveness and resistance to therapy. Although long non-coding RNAs (lncRNAs) are increasingly recognized as major gene ...

P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.
Bugai A, Quaresma AJC, Friedel CC, Lenasi T, Düster R, Sibley CR, Fujinaga K, Kukanja P, Hennig T, Blasius M, Geyer M, Ule J, Dölken L, Barborič M
DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain ill defined. Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcr...

The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.
Tsuda M, Fukuda A, Roy N, Hiramatsu Y, Leonhardt L, Kakiuchi N, Hoyer K, Ogawa S, Goto N, Ikuta K, Kimura Y, Matsumoto Y, Takada Y, Yoshioka T, Maruno T, Yamaga Y, Kim GE, Akiyama H, Ogawa S, Wright CV, Saur D, Takaori K, Uemoto S, Hebrok M, Chiba T, Seno
Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BR...

A new metabolic gene signature in prostate cancer regulated by JMJD3 and EZH2.
Daures M, Idrissou M, Judes G, Rifaï K, Penault-Llorca F, Bignon YJ, Guy L, Bernard-Gallon D
Histone methylation is essential for gene expression control. Trimethylated lysine 27 of histone 3 (H3K27me3) is controlled by the balance between the activities of JMJD3 demethylase and EZH2 methyltransferase. This epigenetic mark has been shown to be deregulated in prostate cancer, and evidence shows H3K27me3 enri...

SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription
Tran N.T. et al.
The structural maintenance of chromosomes (SMC) complex plays an important role in chromosome organization and segregation in most living organisms. In Caulobacter crescentus, SMC is required to align the left and the right arms of the chromosome that run in parallel down the long axis of the cell. However, the...

EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells
Beringer M. et al.
The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding fact...

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  iDeal ChIP-seq kit for Transcription Factors

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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
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<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
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<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
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<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
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<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
			'label2' => 'Species, cell lines, tissues tested',
			'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
			'label3' => 'Additional solutions compatible with iDeal ChIP-seq kit for Transcription Factors',
			'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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			'meta_title' => 'iDeal ChIP-seq kit for Transcription Factors x24',
			'meta_keywords' => '',
			'meta_description' => 'iDeal ChIP-seq kit for Transcription Factors x24',
			'modified' => '2023-06-20 18:27:37',
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			'name' => 'ChIP-qPCR',
			'description' => '<div class="row">
<div class="small-12 medium-12 large-12 columns text-justify">
<p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p>
<p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p>
</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div>
<div class="small-12 medium-12 large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li>
<li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div>
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			'slug' => 'chip-qpcr',
			'meta_keywords' => 'Chromatin immunoprecipitation,ChIP Quantitative PCR,polymerase chain reaction (PCR)',
			'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of',
			'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode',
			'modified' => '2018-01-09 16:46:56',
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<div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div>
<div class="large-12 columns"></div>
<h5 class="large-12 columns"><strong></strong></h5>
<h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div>
<div class="large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink&nbsp;chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by&nbsp;sonication to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with&nbsp;<strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: Reverse&nbsp;cross-links, elute, and purify&nbsp;</li>
<li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify&nbsp;IP'd material</li>
<li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div>
</div>
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			'slug' => 'chromatin-immunoprecipitation-sequencing',
			'meta_keywords' => 'Chromatin Immunoprecipitation Sequencing,ChIP-Seq,ChIP-seq grade antibodies,DNA purification,qPCR,Shearing of chromatin',
			'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing',
			'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation  | Diagenode',
			'modified' => '2017-11-14 09:57:16',
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			'name' => 'Chromatin shearing',
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<div class="small-12 medium-12 large-12 columns">The most important steps for a successful ChIP include both cell fixation and lysis, and chromatin shearing. Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>&reg;</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div>
<div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 &micro;l volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.1 ml Bioruptor&reg; Microtubes (Cat. No. B01200041). <strong>Panel B, 100 &micro;l volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.65 ml Bioruptor&reg; Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 &micro;l volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016).&nbsp;Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37&deg;C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 &micro;l of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div>
<div class="small-12 medium-12 large-12 columns"><br /><br /></div>
<div class="small-12 medium-12 large-12 columns">
<p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p>
</div>
<div class="small-12 medium-12 large-12 columns">
<div class="page" title="Page 7">
<table>
<tbody>
<tr valign="middle">
<td></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>SDS concentration</strong></p>
</td>
<td style="text-align: center;">
<p>&lt; 0.1%</p>
</td>
<td style="text-align: center;">
<p>0.2%</p>
</td>
<td style="text-align: center;">
<p>1%</p>
</td>
<td style="text-align: center;">
<p>0.5%</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Nuclei isolation</strong></p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>No</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Allows for shearing of... cells/tissue</strong></p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>up to 25 g of tissue</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Corresponding to shearing buffers from</strong></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p>
<p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p>
</td>
</tr>
</tbody>
</table>
<p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor&reg; Pico</span></a></em></p>
</div>
</div>
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			'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator',
			'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.',
			'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode',
			'modified' => '2017-11-15 10:14:02',
			'created' => '2015-03-05 15:56:30',
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			'id' => '2',
			'position' => '10',
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			'name' => 'エピジェネティクス・クロマチン解析',
			'description' => '<div class="row">
<div class="large-12 columns">エピジェネティクス研究は、異なる転写パターン、遺伝子発現およびサイレンシングを引き起こすクロマチンの変化に対処します。<br /><br />クロマチンの主成分はDNA<span>およびヒストン蛋白質です。<span>&nbsp;</span></span>各ヒストンコア蛋白質（H2A<span>、</span>H2B<span>、</span>H3<span>および</span>H4<span>）の</span>2<span>つのコピーを</span>8<span>量体に組み込み、</span>DNA<span>で包んでヌクレオソームコアを形成させます。<span>&nbsp;</span></span>ヌクレオソームは、転写機械のDNA<span>への接近可能性および</span>クロマチン再構成因子を制御します。</div>
<div class="large-12 columns">
<p></p>
<p>クロマチン免疫沈降（ChIP<span>）は、関心対象の特定の蛋白質に対するゲノム結合部位の位置を解明するために使用される方法であり、遺伝子発現の制御に関する非常に貴重な洞察を提供します。<span>&nbsp;</span></span>ChIPは特定の抗原を含むクロマチン断片の選択的富化に関与します。 特定の蛋白質または蛋白質修飾を認識する抗体を使用して、特定の遺伝子座における抗原の相対存在量を決定します。</p>
<p>ChIP-seq<span>および</span>ChIP-qPCR<span>は、蛋白質</span>-DNA<span>結合部位の同定を可能にする技術です。</span></p>
<p>&nbsp;</p>
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			'slug' => 'epigenetics-chromatin-study',
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			'meta_description' => 'Diagenodeは、ChIP-Seqおよびクロマチン免疫沈降（ChIP）専用キットと抗体を定量PCRアプリケーションと組み合わせて幅広く提供しています。',
			'meta_title' => 'エピジェネティクス - クロマチン免疫沈降（ChIP）| Diagenode',
			'modified' => '2018-01-11 09:58:47',
			'created' => '2015-02-20 16:10:25',
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			'id' => '81',
			'position' => '2',
			'parent_id' => '5',
			'name' => 'Fixation reagents',
			'description' => '',
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			'in_menu' => false,
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			'hide' => false,
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			'is_antibody' => false,
			'slug' => 'fixatation-reagents',
			'cookies_tag_id' => null,
			'meta_keywords' => 'Fixatation reagents,ChIP cross-link Gold,protein ',
			'meta_description' => 'Diagenode ChIP cross-link Gold for efficient protein stabilization',
			'meta_title' => 'Fixation reagents | Diagenode',
			'modified' => '2019-07-03 10:54:19',
			'created' => '2015-09-16 22:44:10',
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	'Document' => array(
		(int) 0 => array(
			'id' => '134',
			'name' => 'ChIP cross-link Gold',
			'description' => '<div class="page" title="Page 4">
<div class="layoutArea">
<div class="column">
<p><span>The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. Formaldehyde rapidly permeates the cell membranes and enables a fast cross-linking of closely associated proteins in intact cells. However, formaldehyde is usually not effective to cross-link proteins that are not directly bound to the DNA. For example, chromatin interactions with inducible transcription factors or with cofactors that interact with DNA through protein-protein interactions are not well preserve with formaldehyde. So, for higher order and/or dynamic interactions, other cross-linkers should be considered for efficient protein-protein stabilization such as the Diagenode ChIP cross-link Gold. This reagent is to use in combination with formaldehyde. The protocol involves a sequential fixation. A first protein-protein fixation by the ChIP cross-link Gold followed by protein-DNA fixation by formaldehyde. </span></p>
<p><span>Format: </span><span>supplied as a 250 x concentrated solution<br /> </span><span>Shipping conditions</span><span>: shipped at -20&deg;C<br /> </span><span>Storage conditions</span><span>: Store at -20&deg;C; for long storage, store at -80&deg;C. Avoid multiple freeze-thaw cycles. </span></p>
</div>
</div>
</div>',
			'image_id' => null,
			'type' => 'Manual',
			'url' => 'files/products/reagents/ChIP_crosslink_gold_manual.pdf',
			'slug' => 'chip-crosslink-gold-manual',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2016-02-17 12:03:43',
			'created' => '2015-07-07 11:47:43',
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	'Protocol' => array(
		(int) 0 => array(
			'id' => '37',
			'name' => 'Chromatin shearing - Guide for successful chromatin preparation using the Bioruptor<sup>&reg;</sup> Pico',
			'description' => '<p><span>Chromatin immunoprecipitation (ChIP) is a common tool used to study protein-DNA interactions in cells and tissues. The assay can be cumbersome and the success is highly dependent on the quality of chromatin. The first critical step of a successful ChIP experiment is the preparation of sheared chromatin which is representative of the biological scenario of interest. </span></p>',
			'image_id' => '224',
			'type' => 'Protocol',
			'url' => 'files/protocols/bioruptor-pico-chromatin-preparation-guide.pdf',
			'slug' => 'bioruptor-pico-chromatin-preparation-guide',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2017-06-02 11:15:33',
			'created' => '2015-07-20 10:35:07',
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	'Publication' => array(
		(int) 0 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 1 => array(
			'id' => '4793',
			'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.',
			'authors' => 'Paloma S. et al.',
			'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, &gamma;&delta; T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-&kappa;B in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218',
			'doi' => '10.1038/s43587-023-00431-z',
			'modified' => '2023-06-14 15:56:56',
			'created' => '2023-06-13 21:11:31',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '4493',
			'name' => 'Smc5/6 silences episomal transcription by a three-step function.',
			'authors' => 'Abdul  F. et al.',
			'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294',
			'doi' => '10.1038/s41594-022-00829-0',
			'modified' => '2022-11-18 12:41:42',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '4452',
			'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.',
			'authors' => 'Schomann  T. et al.',
			'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://doi.org/10.3390%2Fbiom12081048',
			'doi' => '10.3390/biom12081048',
			'modified' => '2022-10-21 09:33:25',
			'created' => '2022-09-28 09:53:13',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '4240',
			'name' => 'Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer',
			'authors' => 'Schenk MW et al. ',
			'description' => '<p>Small cell lung cancer (SCLC) has a 5-year survival rate of \&lt;7\%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patient-derived explant (CDX) models from donors with extensive stage SCLC to investigate changes at disease progression after chemotherapy. Soluble guanylate cyclase (sGC) is recurrently upregulated in post-chemotherapy progression CDX models, which correlates with acquired chemoresistance. Expression and activation of sGC is regulated by Notch and nitric oxide (NO) signalling with downstream activation of protein kinase G. Genetic targeting of sGC or pharmacological inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing this pathway as a mediator of chemoresistance and potential vulnerability of relapsed SCLC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34789728',
			'doi' => '10.1038/s41467-021-26823-6',
			'modified' => '2022-05-19 17:11:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '4319',
			'name' => 'Regulatory interplay between Vav1, Syk and β-catenin occurs in lungcancer cells.',
			'authors' => 'Boudria Rofia et al. ',
			'description' => '<p>Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. In this study, we show that in lung cancer cells, as such in hematopoietic cells, Vav1 interacts with the Spleen Tyrosine Kinase, Syk. Likewise, Syk interacts with &beta;-catenin and, together with Vav1, regulates the phosphorylation status of &beta;-catenin. Depletion of Vav1, Syk or &beta;-catenin inhibits Rac1 activity and decreases cell migration suggesting the interplay of the three effectors to a common signaling pathway. This model is further supported by the finding that in turn, &beta;-catenin regulates the transcription of Syk gene expression. This study highlights the elaborated connection between Vav1, Syk and &beta;-catenin and the contribution of the trio to cell migration.</p>',
			'date' => '2021-10-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.cellsig.2021.110079',
			'doi' => '10.1016/j.cellsig.2021.110079',
			'modified' => '2022-06-20 09:32:21',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '4171',
			'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.',
			'authors' => 'Ryan, Genevieve E. et al.',
			'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse L&beta;T2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733',
			'doi' => '10.1016/j.mce.2021.111286',
			'modified' => '2021-12-21 15:57:35',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4108',
			'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma',
			'authors' => 'Laubscher et. al.',
			'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that&nbsp;</span><em>SMARCA4</em><span><span>&nbsp;</span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span>&nbsp;</span></span><em>de novo</em><span><span>&nbsp;</span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>',
			'date' => '2021-01-07',
			'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1',
			'doi' => ' 10.21203/rs.3.rs-131009/v1',
			'modified' => '2021-07-07 11:52:23',
			'created' => '2021-07-07 06:38:34',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3997',
			'name' => 'The Human Integrator Complex Facilitates Transcriptional Elongation by Endonucleolytic Cleavage of Nascent Transcripts.',
			'authors' => 'Beckedorff F, Blumenthal E, daSilva LF, Aoi Y, Cingaram PR, Yue J, Zhang A, Dokaneheifard S, Valencia MG, Gaidosh G, Shilatifard A, Shiekhattar R',
			'description' => '<p>Transcription by RNA polymerase II (RNAPII) is pervasive in the human genome. However, the mechanisms controlling transcription at promoters and enhancers remain enigmatic. Here, we demonstrate that Integrator subunit 11 (INTS11), the catalytic subunit of the Integrator complex, regulates transcription at these loci through its endonuclease activity. Promoters of genes require INTS11 to cleave nascent transcripts associated with paused RNAPII and induce their premature termination in the proximity of the&nbsp;+1 nucleosome. The turnover of RNAPII permits the subsequent recruitment of an elongation-competent RNAPII complex, leading to productive elongation. In contrast, enhancers require INTS11 catalysis not to evict paused RNAPII but rather to terminate enhancer RNA transcription beyond the&nbsp;+1 nucleosome. These findings are supported by the differential occupancy of negative elongation factor (NELF), SPT5, and tyrosine-1-phosphorylated RNAPII. This study elucidates the role of Integrator in mediating transcriptional elongation at human promoters through the endonucleolytic cleavage of nascent transcripts and the dynamic turnover of RNAPII.</p>',
			'date' => '2020-07-21',
			'pmid' => 'http://www.pubmed.gov/32697989',
			'doi' => '10.1016/j.celrep.2020.107917',
			'modified' => '2020-09-01 14:44:33',
			'created' => '2020-08-21 16:41:39',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3955',
			'name' => 'Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming.',
			'authors' => 'Suryo Rahmanto Y, Shen W, Shi X, Chen X, Yu Y, Yu ZC, Miyamoto T, Lee MH, Singh V, Asaka R, Shimberg G, Vitolo MI, Martin SS, Wirtz D, Drapkin R, Xuan J, Wang TL, Shih IM',
			'description' => '<p>Somatic inactivating mutations of ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human endometrium-related malignancies. To elucidate the mechanisms underlying how ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murine models with Arid1a and/or Pten&nbsp;conditional deletion in the endometrium. Transcriptomic analyses on endometrial cancers and precursors derived from these mouse&nbsp;models show a close resemblance to human uterine endometrioid carcinomas. We identify transcriptional networks that are controlled by Arid1a and have an impact on endometrial tumor development. To verify findings from the murine models, we analyze ARID1A and ARID1A human endometrial epithelial cells. Using a system biology approach and functional studies, we demonstrate that ARID1A-deficiency lead to loss of TGF-&beta; tumor suppressive function and that inactivation of ARID1A/TGF-&beta; axis promotes migration and invasion of PTEN-deleted endometrial tumor cells. These findings provide molecular insights into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the major causes of cancer mortality.</p>',
			'date' => '2020-06-01',
			'pmid' => 'http://www.pubmed.gov/32483112',
			'doi' => '10.1038/s41467-020-16416-0',
			'modified' => '2020-08-17 09:18:26',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3956',
			'name' => 'AP-1 controls the p11-dependent antidepressant response.',
			'authors' => 'Chottekalapanda RU, Kalik S, Gresack J, Ayala A, Gao M, Wang W, Meller S, Aly A, Schaefer A, Greengard P',
			'description' => '<p>Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations dysregulated during depression. To determine their precise mode of action, we tested whether such neuroadaptive processes are modulated by regulation of specific gene expression programs. Here we identify a transcriptional program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selectively activated prior to the onset of the chronic SSRI response. The AP-1 transcriptional program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response. We find that AP-1 function is required for the antidepressant effect in vivo. Furthermore, we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the antidepressant response. Here we put forth a sequential molecular network to track the antidepressant response and provide a new avenue that could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.</p>',
			'date' => '2020-05-21',
			'pmid' => 'http://www.pubmed.gov/32439846',
			'doi' => '10.1038/s41380-020-0767-8',
			'modified' => '2020-08-17 09:17:39',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3820',
			'name' => 'A stress-responsive enhancer induces dynamic drug resistance in acute myeloid leukemia.',
			'authors' => 'Williams MS, Amaral FM, Simeoni F, Somervaille TC',
			'description' => '<p>The drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts for treatment failure in acute myeloid leukemia (AML). In this study, we identified and functionally validated the network of enhancers that controls expression of ABCB1. We show that exposure of leukemia cells to daunorubicin activated an integrated stress response-like transcriptional program to induce ABCB1 through remodeling and activation of an ATF4-bound, stress-responsive enhancer. Protracted stress primed enhancers for rapid increases in activity following re-exposure of cells to daunorubicin, providing an epigenetic memory of prior drug treatment. In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-responsive enhancer and led to dose-dependent induction of ABCB1. Dynamic induction of ABCB1 by diverse stressors, including chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhibition, providing an explanation for the failure of ABCB1 inhibitors in clinical trials. Stress-induced up regulation of ABCB1 was mitigated by combined use of pharmacologic inhibitors U0126 and ISRIB, which inhibit stress signalling and have potential for use as adjuvants to enhance the activity of ABCB1 inhibitors.</p>',
			'date' => '2019-11-26',
			'pmid' => 'http://www.pubmed.gov/31770110',
			'doi' => '/',
			'modified' => '2020-02-25 13:46:19',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3764',
			'name' => 'The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress.',
			'authors' => 'Moreno Leon L, Gautier M, Allan R, Ilié M, Nottet N, Pons N, Paquet A, Lebrigand K, Truchi M, Fassy J, Magnone V, Kinnebrew G, Radovich M, Cheok MH, Barbry P, Vassaux G, Marquette CH, Ponzio G, Ivan M, Pottier N, Hofman P, Mari B, Rezzonico R',
			'description' => '<p>Lung cancer is the leading cause of cancer death worldwide, with poor prognosis and a high rate of recurrence despite early surgical removal. Hypoxic regions within tumors represent sources of aggressiveness and resistance to therapy. Although long non-coding RNAs (lncRNAs) are increasingly recognized as major gene expression regulators, their regulation and function following hypoxic stress are still largely unexplored. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-&kappa;B and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.</p>',
			'date' => '2019-08-15',
			'pmid' => 'http://www.pubmed.gov/31417181',
			'doi' => '10.1038/s41388-019-0935-y',
			'modified' => '2019-10-03 10:00:42',
			'created' => '2019-10-02 16:16:55',
			'ProductsPublication' => array(
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		),
		(int) 14 => array(
			'id' => '3690',
			'name' => 'P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.',
			'authors' => 'Bugai A, Quaresma AJC, Friedel CC, Lenasi T, Düster R, Sibley CR, Fujinaga K, Kukanja P, Hennig T, Blasius M, Geyer M, Ule J, Dölken L, Barborič M',
			'description' => '<p>DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain ill defined. Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nuclear ribonucleoprotein (7SK snRNP). This is mediated by activation of p38, which triggers enhanced binding of RBM7 with core subunits of 7SK snRNP. In turn, P-TEFb relocates to chromatin to induce transcription of short units, including key DDR genes and multiple classes of non-coding RNAs. Critically, interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-inducing agents due to activation of apoptosis. Our work uncovers the importance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival transcriptional response that is crucial for cell fate upon genotoxic insult.</p>',
			'date' => '2019-04-18',
			'pmid' => 'http://www.pubmed.gov/30824372',
			'doi' => '10.1016/j.molcel.2019.01.033',
			'modified' => '2019-06-28 13:53:03',
			'created' => '2019-06-21 14:55:31',
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		),
		(int) 15 => array(
			'id' => '3597',
			'name' => 'The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.',
			'authors' => 'Tsuda M, Fukuda A, Roy N, Hiramatsu Y, Leonhardt L, Kakiuchi N, Hoyer K, Ogawa S, Goto N, Ikuta K, Kimura Y, Matsumoto Y, Takada Y, Yoshioka T, Maruno T, Yamaga Y, Kim GE, Akiyama H, Ogawa S, Wright CV, Saur D, Takaori K, Uemoto S, Hebrok M, Chiba T, Seno',
			'description' => '<p>Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.</p>',
			'date' => '2018-08-01',
			'pmid' => 'http://www.pubmed.gov/30010625',
			'doi' => '10.1172/JCI94287.',
			'modified' => '2019-04-17 15:09:09',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '3589',
			'name' => 'A new metabolic gene signature in prostate cancer regulated by JMJD3 and EZH2.',
			'authors' => 'Daures M, Idrissou M, Judes G, Rifaï K, Penault-Llorca F, Bignon YJ, Guy L, Bernard-Gallon D',
			'description' => '<p>Histone methylation is essential for gene expression control. Trimethylated lysine 27 of histone 3 (H3K27me3) is controlled by the balance between the activities of JMJD3 demethylase and EZH2 methyltransferase. This epigenetic mark has been shown to be deregulated in prostate cancer, and evidence shows H3K27me3 enrichment on gene promoters in prostate cancer. To study the impact of this enrichment, a transcriptomic analysis with TaqMan Low Density Array (TLDA) of several genes was studied on prostate biopsies divided into three clinical grades: normal ( = 23) and two tumor groups that differed in their aggressiveness (Gleason score &le; 7 ( = 20) and &gt;7 ( = 19)). ANOVA demonstrated that expression of the gene set was upregulated in tumors and correlated with Gleason score, thus discriminating between the three clinical groups. Six genes involved in key cellular processes stood out: , , , , and . Chromatin immunoprecipitation demonstrated collocation of EZH2 and JMJD3 on gene promoters that was dependent on disease stage. Gene set expression was also evaluated on prostate cancer cell lines (DU 145, PC-3 and LNCaP) treated with an inhibitor of JMJD3 (GSK-J4) or EZH2 (DZNeP) to study their involvement in gene regulation. Results showed a difference in GSK-J4 sensitivity under PTEN status of cell lines and an opposite gene expression profile according to androgen status of cells. In summary, our data describe the impacts of JMJD3 and EZH2 on a new gene signature involved in prostate cancer that may help identify diagnostic and therapeutic targets in prostate cancer.</p>',
			'date' => '2018-05-04',
			'pmid' => 'http://www.pubmed.gov/29805743',
			'doi' => '10.18632/oncotarget.25182',
			'modified' => '2019-04-17 15:21:33',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
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		),
		(int) 17 => array(
			'id' => '3272',
			'name' => 'SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription',
			'authors' => 'Tran N.T. et al.',
			'description' => '<p>The structural maintenance of chromosomes (SMC) complex plays an important role in chromosome organization and segregation in most living organisms. In Caulobacter crescentus, SMC is required to align the left and the right arms of the chromosome that run in parallel down the long axis of the cell. However,&nbsp;the mechanism of SMC-mediated alignment of chromosomal arms remains elusive. Here, using genome-wide methods and microscopy of single cells, we show that Caulobacter SMC is recruited to the centromeric parS site and that SMC-mediated arm alignment depends on the chromosome-partitioning protein ParB. We provide evidence that SMC likely tethers the parS-proximal regions of the chromosomal arms together, promoting arm alignment. Furthermore, we show that highly transcribed genes near parS that are oriented against SMC translocation disrupt arm alignment, suggesting that head-on transcription interferes with SMC translocation. Our results demonstrate a tight interdependence of bacterial chromosome organization and global patterns of transcription.</p>',
			'date' => '2017-08-29',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28854358',
			'doi' => '',
			'modified' => '2017-10-16 09:48:59',
			'created' => '2017-10-16 09:48:59',
			'ProductsPublication' => array(
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			'id' => '3105',
			'name' => 'EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells',
			'authors' => 'Beringer M. et al.',
			'description' => '<p>The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding factor at the promoters of bivalent sites. Biochemical and genome-wide analyses show that Elongin BC is associated with Polycomb Repressive Complex 2 (PRC2) in pluripotent stem cells. Elongin BC is recruited to chromatin by the PRC2-associated&nbsp;factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein, also termed C17orf96, esPRC2p48, E130012A19Rik), a protein expressed in the inner cell mass of the mouse blastocyst. Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. Our results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.</p>',
			'date' => '2016-11-17',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27863225',
			'doi' => '',
			'modified' => '2017-01-03 16:02:21',
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            <h6 style="height:60px">iDeal ChIP-seq kit for Transcription Factors</h6>
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'
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	'name' => 'iDeal ChIP-seq kit for Transcription Factors',
	'description' => '<p><a href="https://www.diagenode.com/files/products/kits/ideal-chipseq-transcription-factors-x10-manual.pdf"><img src="https://www.diagenode.com/img/buttons/bt-manual.png" /></a></p>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
<table style="width: 419px; margin-left: auto; margin-right: auto;">
<tbody>
<tr>
<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
</tr>
<tr>
<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
</tr>
<tr>
<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
</tr>
</tbody>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
<p></p>',
	'label1' => 'Characteristics',
	'info1' => '<ul>
<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
</ul>
<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
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<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
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	'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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<p><span>The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. Formaldehyde rapidly permeates the cell membranes and enables a fast cross-linking of closely associated proteins in intact cells. However, formaldehyde is usually not effective to cross-link proteins that are not directly bound to the DNA. For example, chromatin interactions with inducible transcription factors or with cofactors that interact with DNA through protein-protein interactions are not well preserve with formaldehyde. So, for higher order and/or dynamic interactions, other cross-linkers should be considered for efficient protein-protein stabilization such as the Diagenode ChIP cross-link Gold. This reagent is to use in combination with formaldehyde. The protocol involves a sequential fixation. A first protein-protein fixation by the ChIP cross-link Gold followed by protein-DNA fixation by formaldehyde. </span></p>
<p><span>Format: </span><span>supplied as a 250 x concentrated solution<br /> </span><span>Shipping conditions</span><span>: shipped at -20&deg;C<br /> </span><span>Storage conditions</span><span>: Store at -20&deg;C; for long storage, store at -80&deg;C. Avoid multiple freeze-thaw cycles. </span></p>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
</div>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
<table style="width: 419px; margin-left: auto; margin-right: auto;">
<tbody>
<tr>
<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
</tr>
<tr>
<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
</tr>
<tr>
<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
</tr>
</tbody>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
<p></p>',
			'label1' => 'Characteristics',
			'info1' => '<ul>
<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
</ul>
<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
			'label2' => 'Species, cell lines, tissues tested',
			'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
			'label3' => 'Additional solutions compatible with iDeal ChIP-seq kit for Transcription Factors',
			'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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<div class="small-12 medium-12 large-12 columns text-justify">
<p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p>
<p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p>
</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div>
<div class="small-12 medium-12 large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li>
<li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div>
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			'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of',
			'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode',
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<div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div>
<div class="large-12 columns"></div>
<h5 class="large-12 columns"><strong></strong></h5>
<h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div>
<div class="large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink&nbsp;chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by&nbsp;sonication to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with&nbsp;<strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: Reverse&nbsp;cross-links, elute, and purify&nbsp;</li>
<li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify&nbsp;IP'd material</li>
<li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div>
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			'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing',
			'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation  | Diagenode',
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<div class="small-12 medium-12 large-12 columns">The most important steps for a successful ChIP include both cell fixation and lysis, and chromatin shearing. Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>&reg;</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div>
<div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 &micro;l volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.1 ml Bioruptor&reg; Microtubes (Cat. No. B01200041). <strong>Panel B, 100 &micro;l volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.65 ml Bioruptor&reg; Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 &micro;l volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016).&nbsp;Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37&deg;C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 &micro;l of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div>
<div class="small-12 medium-12 large-12 columns"><br /><br /></div>
<div class="small-12 medium-12 large-12 columns">
<p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p>
</div>
<div class="small-12 medium-12 large-12 columns">
<div class="page" title="Page 7">
<table>
<tbody>
<tr valign="middle">
<td></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>SDS concentration</strong></p>
</td>
<td style="text-align: center;">
<p>&lt; 0.1%</p>
</td>
<td style="text-align: center;">
<p>0.2%</p>
</td>
<td style="text-align: center;">
<p>1%</p>
</td>
<td style="text-align: center;">
<p>0.5%</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Nuclei isolation</strong></p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>No</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Allows for shearing of... cells/tissue</strong></p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>up to 25 g of tissue</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Corresponding to shearing buffers from</strong></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p>
<p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p>
</td>
</tr>
</tbody>
</table>
<p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor&reg; Pico</span></a></em></p>
</div>
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			'meta_keywords' => 'Chromatin shearing,Chromatin Immunoprecipitation,Bioruptor,Sonication,Sonicator',
			'meta_description' => 'Diagenode's Bioruptor® is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.',
			'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode',
			'modified' => '2017-11-15 10:14:02',
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			'id' => '2',
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			'parent_id' => null,
			'name' => 'エピジェネティクス・クロマチン解析',
			'description' => '<div class="row">
<div class="large-12 columns">エピジェネティクス研究は、異なる転写パターン、遺伝子発現およびサイレンシングを引き起こすクロマチンの変化に対処します。<br /><br />クロマチンの主成分はDNA<span>およびヒストン蛋白質です。<span>&nbsp;</span></span>各ヒストンコア蛋白質（H2A<span>、</span>H2B<span>、</span>H3<span>および</span>H4<span>）の</span>2<span>つのコピーを</span>8<span>量体に組み込み、</span>DNA<span>で包んでヌクレオソームコアを形成させます。<span>&nbsp;</span></span>ヌクレオソームは、転写機械のDNA<span>への接近可能性および</span>クロマチン再構成因子を制御します。</div>
<div class="large-12 columns">
<p></p>
<p>クロマチン免疫沈降（ChIP<span>）は、関心対象の特定の蛋白質に対するゲノム結合部位の位置を解明するために使用される方法であり、遺伝子発現の制御に関する非常に貴重な洞察を提供します。<span>&nbsp;</span></span>ChIPは特定の抗原を含むクロマチン断片の選択的富化に関与します。 特定の蛋白質または蛋白質修飾を認識する抗体を使用して、特定の遺伝子座における抗原の相対存在量を決定します。</p>
<p>ChIP-seq<span>および</span>ChIP-qPCR<span>は、蛋白質</span>-DNA<span>結合部位の同定を可能にする技術です。</span></p>
<p>&nbsp;</p>
</div>
</div>',
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			'meta_description' => 'Diagenodeは、ChIP-Seqおよびクロマチン免疫沈降（ChIP）専用キットと抗体を定量PCRアプリケーションと組み合わせて幅広く提供しています。',
			'meta_title' => 'エピジェネティクス - クロマチン免疫沈降（ChIP）| Diagenode',
			'modified' => '2018-01-11 09:58:47',
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			'name' => 'Fixation reagents',
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			'meta_keywords' => 'Fixatation reagents,ChIP cross-link Gold,protein ',
			'meta_description' => 'Diagenode ChIP cross-link Gold for efficient protein stabilization',
			'meta_title' => 'Fixation reagents | Diagenode',
			'modified' => '2019-07-03 10:54:19',
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			'name' => 'ChIP cross-link Gold',
			'description' => '<div class="page" title="Page 4">
<div class="layoutArea">
<div class="column">
<p><span>The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. Formaldehyde rapidly permeates the cell membranes and enables a fast cross-linking of closely associated proteins in intact cells. However, formaldehyde is usually not effective to cross-link proteins that are not directly bound to the DNA. For example, chromatin interactions with inducible transcription factors or with cofactors that interact with DNA through protein-protein interactions are not well preserve with formaldehyde. So, for higher order and/or dynamic interactions, other cross-linkers should be considered for efficient protein-protein stabilization such as the Diagenode ChIP cross-link Gold. This reagent is to use in combination with formaldehyde. The protocol involves a sequential fixation. A first protein-protein fixation by the ChIP cross-link Gold followed by protein-DNA fixation by formaldehyde. </span></p>
<p><span>Format: </span><span>supplied as a 250 x concentrated solution<br /> </span><span>Shipping conditions</span><span>: shipped at -20&deg;C<br /> </span><span>Storage conditions</span><span>: Store at -20&deg;C; for long storage, store at -80&deg;C. Avoid multiple freeze-thaw cycles. </span></p>
</div>
</div>
</div>',
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			'type' => 'Manual',
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			'slug' => 'chip-crosslink-gold-manual',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2016-02-17 12:03:43',
			'created' => '2015-07-07 11:47:43',
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		(int) 0 => array(
			'id' => '37',
			'name' => 'Chromatin shearing - Guide for successful chromatin preparation using the Bioruptor<sup>&reg;</sup> Pico',
			'description' => '<p><span>Chromatin immunoprecipitation (ChIP) is a common tool used to study protein-DNA interactions in cells and tissues. The assay can be cumbersome and the success is highly dependent on the quality of chromatin. The first critical step of a successful ChIP experiment is the preparation of sheared chromatin which is representative of the biological scenario of interest. </span></p>',
			'image_id' => '224',
			'type' => 'Protocol',
			'url' => 'files/protocols/bioruptor-pico-chromatin-preparation-guide.pdf',
			'slug' => 'bioruptor-pico-chromatin-preparation-guide',
			'meta_keywords' => '',
			'meta_description' => '',
			'modified' => '2017-06-02 11:15:33',
			'created' => '2015-07-20 10:35:07',
			'ProductsProtocol' => array(
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			)
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	),
	'Publication' => array(
		(int) 0 => array(
			'id' => '4843',
			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
			'modified' => '2023-08-01 14:14:01',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 1 => array(
			'id' => '4793',
			'name' => 'Targeting lymphoid-derived IL-17 signaling to delay skin aging.',
			'authors' => 'Paloma S. et al.',
			'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, &gamma;&delta; T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-&kappa;B in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218',
			'doi' => '10.1038/s43587-023-00431-z',
			'modified' => '2023-06-14 15:56:56',
			'created' => '2023-06-13 21:11:31',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 2 => array(
			'id' => '4862',
			'name' => 'Mutant FUS induces chromatin reorganization in the hippocampus andalters memory processes.',
			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
			'modified' => '2023-08-01 14:55:49',
			'created' => '2023-08-01 15:59:38',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 3 => array(
			'id' => '4493',
			'name' => 'Smc5/6 silences episomal transcription by a three-step function.',
			'authors' => 'Abdul  F. et al.',
			'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>',
			'date' => '2022-09-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/36097294',
			'doi' => '10.1038/s41594-022-00829-0',
			'modified' => '2022-11-18 12:41:42',
			'created' => '2022-11-15 09:26:20',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 4 => array(
			'id' => '4452',
			'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.',
			'authors' => 'Schomann  T. et al.',
			'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://doi.org/10.3390%2Fbiom12081048',
			'doi' => '10.3390/biom12081048',
			'modified' => '2022-10-21 09:33:25',
			'created' => '2022-09-28 09:53:13',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '4240',
			'name' => 'Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer',
			'authors' => 'Schenk MW et al. ',
			'description' => '<p>Small cell lung cancer (SCLC) has a 5-year survival rate of \&lt;7\%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patient-derived explant (CDX) models from donors with extensive stage SCLC to investigate changes at disease progression after chemotherapy. Soluble guanylate cyclase (sGC) is recurrently upregulated in post-chemotherapy progression CDX models, which correlates with acquired chemoresistance. Expression and activation of sGC is regulated by Notch and nitric oxide (NO) signalling with downstream activation of protein kinase G. Genetic targeting of sGC or pharmacological inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing this pathway as a mediator of chemoresistance and potential vulnerability of relapsed SCLC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34789728',
			'doi' => '10.1038/s41467-021-26823-6',
			'modified' => '2022-05-19 17:11:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '4319',
			'name' => 'Regulatory interplay between Vav1, Syk and β-catenin occurs in lungcancer cells.',
			'authors' => 'Boudria Rofia et al. ',
			'description' => '<p>Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. In this study, we show that in lung cancer cells, as such in hematopoietic cells, Vav1 interacts with the Spleen Tyrosine Kinase, Syk. Likewise, Syk interacts with &beta;-catenin and, together with Vav1, regulates the phosphorylation status of &beta;-catenin. Depletion of Vav1, Syk or &beta;-catenin inhibits Rac1 activity and decreases cell migration suggesting the interplay of the three effectors to a common signaling pathway. This model is further supported by the finding that in turn, &beta;-catenin regulates the transcription of Syk gene expression. This study highlights the elaborated connection between Vav1, Syk and &beta;-catenin and the contribution of the trio to cell migration.</p>',
			'date' => '2021-10-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.cellsig.2021.110079',
			'doi' => '10.1016/j.cellsig.2021.110079',
			'modified' => '2022-06-20 09:32:21',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '4171',
			'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.',
			'authors' => 'Ryan, Genevieve E. et al.',
			'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse L&beta;T2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733',
			'doi' => '10.1016/j.mce.2021.111286',
			'modified' => '2021-12-21 15:57:35',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4108',
			'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma',
			'authors' => 'Laubscher et. al.',
			'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that&nbsp;</span><em>SMARCA4</em><span><span>&nbsp;</span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span>&nbsp;</span></span><em>de novo</em><span><span>&nbsp;</span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>',
			'date' => '2021-01-07',
			'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1',
			'doi' => ' 10.21203/rs.3.rs-131009/v1',
			'modified' => '2021-07-07 11:52:23',
			'created' => '2021-07-07 06:38:34',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3997',
			'name' => 'The Human Integrator Complex Facilitates Transcriptional Elongation by Endonucleolytic Cleavage of Nascent Transcripts.',
			'authors' => 'Beckedorff F, Blumenthal E, daSilva LF, Aoi Y, Cingaram PR, Yue J, Zhang A, Dokaneheifard S, Valencia MG, Gaidosh G, Shilatifard A, Shiekhattar R',
			'description' => '<p>Transcription by RNA polymerase II (RNAPII) is pervasive in the human genome. However, the mechanisms controlling transcription at promoters and enhancers remain enigmatic. Here, we demonstrate that Integrator subunit 11 (INTS11), the catalytic subunit of the Integrator complex, regulates transcription at these loci through its endonuclease activity. Promoters of genes require INTS11 to cleave nascent transcripts associated with paused RNAPII and induce their premature termination in the proximity of the&nbsp;+1 nucleosome. The turnover of RNAPII permits the subsequent recruitment of an elongation-competent RNAPII complex, leading to productive elongation. In contrast, enhancers require INTS11 catalysis not to evict paused RNAPII but rather to terminate enhancer RNA transcription beyond the&nbsp;+1 nucleosome. These findings are supported by the differential occupancy of negative elongation factor (NELF), SPT5, and tyrosine-1-phosphorylated RNAPII. This study elucidates the role of Integrator in mediating transcriptional elongation at human promoters through the endonucleolytic cleavage of nascent transcripts and the dynamic turnover of RNAPII.</p>',
			'date' => '2020-07-21',
			'pmid' => 'http://www.pubmed.gov/32697989',
			'doi' => '10.1016/j.celrep.2020.107917',
			'modified' => '2020-09-01 14:44:33',
			'created' => '2020-08-21 16:41:39',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3955',
			'name' => 'Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming.',
			'authors' => 'Suryo Rahmanto Y, Shen W, Shi X, Chen X, Yu Y, Yu ZC, Miyamoto T, Lee MH, Singh V, Asaka R, Shimberg G, Vitolo MI, Martin SS, Wirtz D, Drapkin R, Xuan J, Wang TL, Shih IM',
			'description' => '<p>Somatic inactivating mutations of ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human endometrium-related malignancies. To elucidate the mechanisms underlying how ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murine models with Arid1a and/or Pten&nbsp;conditional deletion in the endometrium. Transcriptomic analyses on endometrial cancers and precursors derived from these mouse&nbsp;models show a close resemblance to human uterine endometrioid carcinomas. We identify transcriptional networks that are controlled by Arid1a and have an impact on endometrial tumor development. To verify findings from the murine models, we analyze ARID1A and ARID1A human endometrial epithelial cells. Using a system biology approach and functional studies, we demonstrate that ARID1A-deficiency lead to loss of TGF-&beta; tumor suppressive function and that inactivation of ARID1A/TGF-&beta; axis promotes migration and invasion of PTEN-deleted endometrial tumor cells. These findings provide molecular insights into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the major causes of cancer mortality.</p>',
			'date' => '2020-06-01',
			'pmid' => 'http://www.pubmed.gov/32483112',
			'doi' => '10.1038/s41467-020-16416-0',
			'modified' => '2020-08-17 09:18:26',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3956',
			'name' => 'AP-1 controls the p11-dependent antidepressant response.',
			'authors' => 'Chottekalapanda RU, Kalik S, Gresack J, Ayala A, Gao M, Wang W, Meller S, Aly A, Schaefer A, Greengard P',
			'description' => '<p>Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations dysregulated during depression. To determine their precise mode of action, we tested whether such neuroadaptive processes are modulated by regulation of specific gene expression programs. Here we identify a transcriptional program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selectively activated prior to the onset of the chronic SSRI response. The AP-1 transcriptional program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response. We find that AP-1 function is required for the antidepressant effect in vivo. Furthermore, we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the antidepressant response. Here we put forth a sequential molecular network to track the antidepressant response and provide a new avenue that could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.</p>',
			'date' => '2020-05-21',
			'pmid' => 'http://www.pubmed.gov/32439846',
			'doi' => '10.1038/s41380-020-0767-8',
			'modified' => '2020-08-17 09:17:39',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
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		),
		(int) 12 => array(
			'id' => '3820',
			'name' => 'A stress-responsive enhancer induces dynamic drug resistance in acute myeloid leukemia.',
			'authors' => 'Williams MS, Amaral FM, Simeoni F, Somervaille TC',
			'description' => '<p>The drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts for treatment failure in acute myeloid leukemia (AML). In this study, we identified and functionally validated the network of enhancers that controls expression of ABCB1. We show that exposure of leukemia cells to daunorubicin activated an integrated stress response-like transcriptional program to induce ABCB1 through remodeling and activation of an ATF4-bound, stress-responsive enhancer. Protracted stress primed enhancers for rapid increases in activity following re-exposure of cells to daunorubicin, providing an epigenetic memory of prior drug treatment. In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-responsive enhancer and led to dose-dependent induction of ABCB1. Dynamic induction of ABCB1 by diverse stressors, including chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhibition, providing an explanation for the failure of ABCB1 inhibitors in clinical trials. Stress-induced up regulation of ABCB1 was mitigated by combined use of pharmacologic inhibitors U0126 and ISRIB, which inhibit stress signalling and have potential for use as adjuvants to enhance the activity of ABCB1 inhibitors.</p>',
			'date' => '2019-11-26',
			'pmid' => 'http://www.pubmed.gov/31770110',
			'doi' => '/',
			'modified' => '2020-02-25 13:46:19',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3764',
			'name' => 'The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress.',
			'authors' => 'Moreno Leon L, Gautier M, Allan R, Ilié M, Nottet N, Pons N, Paquet A, Lebrigand K, Truchi M, Fassy J, Magnone V, Kinnebrew G, Radovich M, Cheok MH, Barbry P, Vassaux G, Marquette CH, Ponzio G, Ivan M, Pottier N, Hofman P, Mari B, Rezzonico R',
			'description' => '<p>Lung cancer is the leading cause of cancer death worldwide, with poor prognosis and a high rate of recurrence despite early surgical removal. Hypoxic regions within tumors represent sources of aggressiveness and resistance to therapy. Although long non-coding RNAs (lncRNAs) are increasingly recognized as major gene expression regulators, their regulation and function following hypoxic stress are still largely unexplored. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-&kappa;B and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.</p>',
			'date' => '2019-08-15',
			'pmid' => 'http://www.pubmed.gov/31417181',
			'doi' => '10.1038/s41388-019-0935-y',
			'modified' => '2019-10-03 10:00:42',
			'created' => '2019-10-02 16:16:55',
			'ProductsPublication' => array(
				[maximum depth reached]
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		),
		(int) 14 => array(
			'id' => '3690',
			'name' => 'P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.',
			'authors' => 'Bugai A, Quaresma AJC, Friedel CC, Lenasi T, Düster R, Sibley CR, Fujinaga K, Kukanja P, Hennig T, Blasius M, Geyer M, Ule J, Dölken L, Barborič M',
			'description' => '<p>DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain ill defined. Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nuclear ribonucleoprotein (7SK snRNP). This is mediated by activation of p38, which triggers enhanced binding of RBM7 with core subunits of 7SK snRNP. In turn, P-TEFb relocates to chromatin to induce transcription of short units, including key DDR genes and multiple classes of non-coding RNAs. Critically, interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-inducing agents due to activation of apoptosis. Our work uncovers the importance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival transcriptional response that is crucial for cell fate upon genotoxic insult.</p>',
			'date' => '2019-04-18',
			'pmid' => 'http://www.pubmed.gov/30824372',
			'doi' => '10.1016/j.molcel.2019.01.033',
			'modified' => '2019-06-28 13:53:03',
			'created' => '2019-06-21 14:55:31',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3597',
			'name' => 'The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.',
			'authors' => 'Tsuda M, Fukuda A, Roy N, Hiramatsu Y, Leonhardt L, Kakiuchi N, Hoyer K, Ogawa S, Goto N, Ikuta K, Kimura Y, Matsumoto Y, Takada Y, Yoshioka T, Maruno T, Yamaga Y, Kim GE, Akiyama H, Ogawa S, Wright CV, Saur D, Takaori K, Uemoto S, Hebrok M, Chiba T, Seno',
			'description' => '<p>Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.</p>',
			'date' => '2018-08-01',
			'pmid' => 'http://www.pubmed.gov/30010625',
			'doi' => '10.1172/JCI94287.',
			'modified' => '2019-04-17 15:09:09',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '3589',
			'name' => 'A new metabolic gene signature in prostate cancer regulated by JMJD3 and EZH2.',
			'authors' => 'Daures M, Idrissou M, Judes G, Rifaï K, Penault-Llorca F, Bignon YJ, Guy L, Bernard-Gallon D',
			'description' => '<p>Histone methylation is essential for gene expression control. Trimethylated lysine 27 of histone 3 (H3K27me3) is controlled by the balance between the activities of JMJD3 demethylase and EZH2 methyltransferase. This epigenetic mark has been shown to be deregulated in prostate cancer, and evidence shows H3K27me3 enrichment on gene promoters in prostate cancer. To study the impact of this enrichment, a transcriptomic analysis with TaqMan Low Density Array (TLDA) of several genes was studied on prostate biopsies divided into three clinical grades: normal ( = 23) and two tumor groups that differed in their aggressiveness (Gleason score &le; 7 ( = 20) and &gt;7 ( = 19)). ANOVA demonstrated that expression of the gene set was upregulated in tumors and correlated with Gleason score, thus discriminating between the three clinical groups. Six genes involved in key cellular processes stood out: , , , , and . Chromatin immunoprecipitation demonstrated collocation of EZH2 and JMJD3 on gene promoters that was dependent on disease stage. Gene set expression was also evaluated on prostate cancer cell lines (DU 145, PC-3 and LNCaP) treated with an inhibitor of JMJD3 (GSK-J4) or EZH2 (DZNeP) to study their involvement in gene regulation. Results showed a difference in GSK-J4 sensitivity under PTEN status of cell lines and an opposite gene expression profile according to androgen status of cells. In summary, our data describe the impacts of JMJD3 and EZH2 on a new gene signature involved in prostate cancer that may help identify diagnostic and therapeutic targets in prostate cancer.</p>',
			'date' => '2018-05-04',
			'pmid' => 'http://www.pubmed.gov/29805743',
			'doi' => '10.18632/oncotarget.25182',
			'modified' => '2019-04-17 15:21:33',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '3272',
			'name' => 'SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription',
			'authors' => 'Tran N.T. et al.',
			'description' => '<p>The structural maintenance of chromosomes (SMC) complex plays an important role in chromosome organization and segregation in most living organisms. In Caulobacter crescentus, SMC is required to align the left and the right arms of the chromosome that run in parallel down the long axis of the cell. However,&nbsp;the mechanism of SMC-mediated alignment of chromosomal arms remains elusive. Here, using genome-wide methods and microscopy of single cells, we show that Caulobacter SMC is recruited to the centromeric parS site and that SMC-mediated arm alignment depends on the chromosome-partitioning protein ParB. We provide evidence that SMC likely tethers the parS-proximal regions of the chromosomal arms together, promoting arm alignment. Furthermore, we show that highly transcribed genes near parS that are oriented against SMC translocation disrupt arm alignment, suggesting that head-on transcription interferes with SMC translocation. Our results demonstrate a tight interdependence of bacterial chromosome organization and global patterns of transcription.</p>',
			'date' => '2017-08-29',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28854358',
			'doi' => '',
			'modified' => '2017-10-16 09:48:59',
			'created' => '2017-10-16 09:48:59',
			'ProductsPublication' => array(
				[maximum depth reached]
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		(int) 18 => array(
			'id' => '3105',
			'name' => 'EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells',
			'authors' => 'Beringer M. et al.',
			'description' => '<p>The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding factor at the promoters of bivalent sites. Biochemical and genome-wide analyses show that Elongin BC is associated with Polycomb Repressive Complex 2 (PRC2) in pluripotent stem cells. Elongin BC is recruited to chromatin by the PRC2-associated&nbsp;factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein, also termed C17orf96, esPRC2p48, E130012A19Rik), a protein expressed in the inner cell mass of the mouse blastocyst. Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. Our results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.</p>',
			'date' => '2016-11-17',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27863225',
			'doi' => '',
			'modified' => '2017-01-03 16:02:21',
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            <h6 style="height:60px">iDeal ChIP-seq kit for Transcription Factors</h6>
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	'description' => '<p><a href="https://www.diagenode.com/files/products/kits/ideal-chipseq-transcription-factors-x10-manual.pdf"><img src="https://www.diagenode.com/img/buttons/bt-manual.png" /></a></p>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
<table style="width: 419px; margin-left: auto; margin-right: auto;">
<tbody>
<tr>
<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
</tr>
<tr>
<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
</tr>
<tr>
<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
</tr>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
<p></p>',
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
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<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
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	'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
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	'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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		'description' => '<p style="text-align: justify;"><span>Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. However, formaldehyde is usually not effective&nbsp;</span><span>in cross-linking</span><span>&nbsp;proteins that are not directly bound to the DNA.</span><span>&nbsp;</span><span>For example, inducible transcription factors or cofactors interact with DNA through protein-protein interactions, and these are not well preserved with formaldehyde. F</span><span>or such higher order and/or dynamic interactions such as this, other cross-linkers should be considered for efficient protein-protein stabilization. Diagenode's ChIP cross-link Gold which is</span><span>&nbsp;used in combination with formaldehyde is an excellent choice for such higher order protein interactions.&nbsp;</span></p>',
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			'name' => 'iDeal ChIP-seq kit for Transcription Factors',
			'description' => '<p><a href="https://www.diagenode.com/files/products/kits/ideal-chipseq-transcription-factors-x10-manual.pdf"><img src="https://www.diagenode.com/img/buttons/bt-manual.png" /></a></p>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
<table style="width: 419px; margin-left: auto; margin-right: auto;">
<tbody>
<tr>
<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
</tr>
<tr>
<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
</tr>
<tr>
<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
</tr>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
<p></p>',
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
</ul>
<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
			'label2' => 'Species, cell lines, tissues tested',
			'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
			'label3' => 'Additional solutions compatible with iDeal ChIP-seq kit for Transcription Factors',
			'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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<div class="small-12 medium-12 large-12 columns text-justify">
<p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p>
<p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p>
</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div>
<div class="small-12 medium-12 large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li>
<li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div>
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			'meta_description' => 'Diagenode's ChIP qPCR kits can be used to quantify enriched DNA after chromatin immunoprecipitation. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of',
			'meta_title' => 'ChIP Quantitative PCR (ChIP-qPCR) | Diagenode',
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<div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div>
<div class="large-12 columns"></div>
<h5 class="large-12 columns"><strong></strong></h5>
<h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div>
<div class="large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink&nbsp;chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by&nbsp;sonication to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with&nbsp;<strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: Reverse&nbsp;cross-links, elute, and purify&nbsp;</li>
<li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify&nbsp;IP'd material</li>
<li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div>
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			'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing',
			'meta_title' => 'Chromatin Immunoprecipitation - ChIP-seq Kits - Dna methylation  | Diagenode',
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			'name' => 'Chromatin shearing',
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<div class="small-12 medium-12 large-12 columns">The most important steps for a successful ChIP include both cell fixation and lysis, and chromatin shearing. Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>&reg;</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div>
<div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 &micro;l volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.1 ml Bioruptor&reg; Microtubes (Cat. No. B01200041). <strong>Panel B, 100 &micro;l volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.65 ml Bioruptor&reg; Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 &micro;l volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016).&nbsp;Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37&deg;C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 &micro;l of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div>
<div class="small-12 medium-12 large-12 columns"><br /><br /></div>
<div class="small-12 medium-12 large-12 columns">
<p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p>
</div>
<div class="small-12 medium-12 large-12 columns">
<div class="page" title="Page 7">
<table>
<tbody>
<tr valign="middle">
<td></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>SDS concentration</strong></p>
</td>
<td style="text-align: center;">
<p>&lt; 0.1%</p>
</td>
<td style="text-align: center;">
<p>0.2%</p>
</td>
<td style="text-align: center;">
<p>1%</p>
</td>
<td style="text-align: center;">
<p>0.5%</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Nuclei isolation</strong></p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>No</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Allows for shearing of... cells/tissue</strong></p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>up to 25 g of tissue</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Corresponding to shearing buffers from</strong></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p>
<p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p>
</td>
</tr>
</tbody>
</table>
<p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor&reg; Pico</span></a></em></p>
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			'name' => 'エピジェネティクス・クロマチン解析',
			'description' => '<div class="row">
<div class="large-12 columns">エピジェネティクス研究は、異なる転写パターン、遺伝子発現およびサイレンシングを引き起こすクロマチンの変化に対処します。<br /><br />クロマチンの主成分はDNA<span>およびヒストン蛋白質です。<span>&nbsp;</span></span>各ヒストンコア蛋白質（H2A<span>、</span>H2B<span>、</span>H3<span>および</span>H4<span>）の</span>2<span>つのコピーを</span>8<span>量体に組み込み、</span>DNA<span>で包んでヌクレオソームコアを形成させます。<span>&nbsp;</span></span>ヌクレオソームは、転写機械のDNA<span>への接近可能性および</span>クロマチン再構成因子を制御します。</div>
<div class="large-12 columns">
<p></p>
<p>クロマチン免疫沈降（ChIP<span>）は、関心対象の特定の蛋白質に対するゲノム結合部位の位置を解明するために使用される方法であり、遺伝子発現の制御に関する非常に貴重な洞察を提供します。<span>&nbsp;</span></span>ChIPは特定の抗原を含むクロマチン断片の選択的富化に関与します。 特定の蛋白質または蛋白質修飾を認識する抗体を使用して、特定の遺伝子座における抗原の相対存在量を決定します。</p>
<p>ChIP-seq<span>および</span>ChIP-qPCR<span>は、蛋白質</span>-DNA<span>結合部位の同定を可能にする技術です。</span></p>
<p>&nbsp;</p>
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<p><span>The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. Formaldehyde rapidly permeates the cell membranes and enables a fast cross-linking of closely associated proteins in intact cells. However, formaldehyde is usually not effective to cross-link proteins that are not directly bound to the DNA. For example, chromatin interactions with inducible transcription factors or with cofactors that interact with DNA through protein-protein interactions are not well preserve with formaldehyde. So, for higher order and/or dynamic interactions, other cross-linkers should be considered for efficient protein-protein stabilization such as the Diagenode ChIP cross-link Gold. This reagent is to use in combination with formaldehyde. The protocol involves a sequential fixation. A first protein-protein fixation by the ChIP cross-link Gold followed by protein-DNA fixation by formaldehyde. </span></p>
<p><span>Format: </span><span>supplied as a 250 x concentrated solution<br /> </span><span>Shipping conditions</span><span>: shipped at -20&deg;C<br /> </span><span>Storage conditions</span><span>: Store at -20&deg;C; for long storage, store at -80&deg;C. Avoid multiple freeze-thaw cycles. </span></p>
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			'name' => 'Chromatin shearing - Guide for successful chromatin preparation using the Bioruptor<sup>&reg;</sup> Pico',
			'description' => '<p><span>Chromatin immunoprecipitation (ChIP) is a common tool used to study protein-DNA interactions in cells and tissues. The assay can be cumbersome and the success is highly dependent on the quality of chromatin. The first critical step of a successful ChIP experiment is the preparation of sheared chromatin which is representative of the biological scenario of interest. </span></p>',
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			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
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			'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, &gamma;&delta; T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-&kappa;B in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218',
			'doi' => '10.1038/s43587-023-00431-z',
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			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37327984',
			'doi' => '10.1016/j.pneurobio.2023.102483',
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			'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>',
			'date' => '2022-09-01',
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			'doi' => '10.1038/s41594-022-00829-0',
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			'authors' => 'Schomann  T. et al.',
			'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://doi.org/10.3390%2Fbiom12081048',
			'doi' => '10.3390/biom12081048',
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			'name' => 'Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer',
			'authors' => 'Schenk MW et al. ',
			'description' => '<p>Small cell lung cancer (SCLC) has a 5-year survival rate of \&lt;7\%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patient-derived explant (CDX) models from donors with extensive stage SCLC to investigate changes at disease progression after chemotherapy. Soluble guanylate cyclase (sGC) is recurrently upregulated in post-chemotherapy progression CDX models, which correlates with acquired chemoresistance. Expression and activation of sGC is regulated by Notch and nitric oxide (NO) signalling with downstream activation of protein kinase G. Genetic targeting of sGC or pharmacological inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing this pathway as a mediator of chemoresistance and potential vulnerability of relapsed SCLC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34789728',
			'doi' => '10.1038/s41467-021-26823-6',
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			'name' => 'Regulatory interplay between Vav1, Syk and β-catenin occurs in lungcancer cells.',
			'authors' => 'Boudria Rofia et al. ',
			'description' => '<p>Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. In this study, we show that in lung cancer cells, as such in hematopoietic cells, Vav1 interacts with the Spleen Tyrosine Kinase, Syk. Likewise, Syk interacts with &beta;-catenin and, together with Vav1, regulates the phosphorylation status of &beta;-catenin. Depletion of Vav1, Syk or &beta;-catenin inhibits Rac1 activity and decreases cell migration suggesting the interplay of the three effectors to a common signaling pathway. This model is further supported by the finding that in turn, &beta;-catenin regulates the transcription of Syk gene expression. This study highlights the elaborated connection between Vav1, Syk and &beta;-catenin and the contribution of the trio to cell migration.</p>',
			'date' => '2021-10-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.cellsig.2021.110079',
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			'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.',
			'authors' => 'Ryan, Genevieve E. et al.',
			'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse L&beta;T2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733',
			'doi' => '10.1016/j.mce.2021.111286',
			'modified' => '2021-12-21 15:57:35',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4108',
			'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma',
			'authors' => 'Laubscher et. al.',
			'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that&nbsp;</span><em>SMARCA4</em><span><span>&nbsp;</span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span>&nbsp;</span></span><em>de novo</em><span><span>&nbsp;</span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>',
			'date' => '2021-01-07',
			'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1',
			'doi' => ' 10.21203/rs.3.rs-131009/v1',
			'modified' => '2021-07-07 11:52:23',
			'created' => '2021-07-07 06:38:34',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3997',
			'name' => 'The Human Integrator Complex Facilitates Transcriptional Elongation by Endonucleolytic Cleavage of Nascent Transcripts.',
			'authors' => 'Beckedorff F, Blumenthal E, daSilva LF, Aoi Y, Cingaram PR, Yue J, Zhang A, Dokaneheifard S, Valencia MG, Gaidosh G, Shilatifard A, Shiekhattar R',
			'description' => '<p>Transcription by RNA polymerase II (RNAPII) is pervasive in the human genome. However, the mechanisms controlling transcription at promoters and enhancers remain enigmatic. Here, we demonstrate that Integrator subunit 11 (INTS11), the catalytic subunit of the Integrator complex, regulates transcription at these loci through its endonuclease activity. Promoters of genes require INTS11 to cleave nascent transcripts associated with paused RNAPII and induce their premature termination in the proximity of the&nbsp;+1 nucleosome. The turnover of RNAPII permits the subsequent recruitment of an elongation-competent RNAPII complex, leading to productive elongation. In contrast, enhancers require INTS11 catalysis not to evict paused RNAPII but rather to terminate enhancer RNA transcription beyond the&nbsp;+1 nucleosome. These findings are supported by the differential occupancy of negative elongation factor (NELF), SPT5, and tyrosine-1-phosphorylated RNAPII. This study elucidates the role of Integrator in mediating transcriptional elongation at human promoters through the endonucleolytic cleavage of nascent transcripts and the dynamic turnover of RNAPII.</p>',
			'date' => '2020-07-21',
			'pmid' => 'http://www.pubmed.gov/32697989',
			'doi' => '10.1016/j.celrep.2020.107917',
			'modified' => '2020-09-01 14:44:33',
			'created' => '2020-08-21 16:41:39',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3955',
			'name' => 'Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming.',
			'authors' => 'Suryo Rahmanto Y, Shen W, Shi X, Chen X, Yu Y, Yu ZC, Miyamoto T, Lee MH, Singh V, Asaka R, Shimberg G, Vitolo MI, Martin SS, Wirtz D, Drapkin R, Xuan J, Wang TL, Shih IM',
			'description' => '<p>Somatic inactivating mutations of ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human endometrium-related malignancies. To elucidate the mechanisms underlying how ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murine models with Arid1a and/or Pten&nbsp;conditional deletion in the endometrium. Transcriptomic analyses on endometrial cancers and precursors derived from these mouse&nbsp;models show a close resemblance to human uterine endometrioid carcinomas. We identify transcriptional networks that are controlled by Arid1a and have an impact on endometrial tumor development. To verify findings from the murine models, we analyze ARID1A and ARID1A human endometrial epithelial cells. Using a system biology approach and functional studies, we demonstrate that ARID1A-deficiency lead to loss of TGF-&beta; tumor suppressive function and that inactivation of ARID1A/TGF-&beta; axis promotes migration and invasion of PTEN-deleted endometrial tumor cells. These findings provide molecular insights into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the major causes of cancer mortality.</p>',
			'date' => '2020-06-01',
			'pmid' => 'http://www.pubmed.gov/32483112',
			'doi' => '10.1038/s41467-020-16416-0',
			'modified' => '2020-08-17 09:18:26',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3956',
			'name' => 'AP-1 controls the p11-dependent antidepressant response.',
			'authors' => 'Chottekalapanda RU, Kalik S, Gresack J, Ayala A, Gao M, Wang W, Meller S, Aly A, Schaefer A, Greengard P',
			'description' => '<p>Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations dysregulated during depression. To determine their precise mode of action, we tested whether such neuroadaptive processes are modulated by regulation of specific gene expression programs. Here we identify a transcriptional program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selectively activated prior to the onset of the chronic SSRI response. The AP-1 transcriptional program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response. We find that AP-1 function is required for the antidepressant effect in vivo. Furthermore, we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the antidepressant response. Here we put forth a sequential molecular network to track the antidepressant response and provide a new avenue that could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.</p>',
			'date' => '2020-05-21',
			'pmid' => 'http://www.pubmed.gov/32439846',
			'doi' => '10.1038/s41380-020-0767-8',
			'modified' => '2020-08-17 09:17:39',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3820',
			'name' => 'A stress-responsive enhancer induces dynamic drug resistance in acute myeloid leukemia.',
			'authors' => 'Williams MS, Amaral FM, Simeoni F, Somervaille TC',
			'description' => '<p>The drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts for treatment failure in acute myeloid leukemia (AML). In this study, we identified and functionally validated the network of enhancers that controls expression of ABCB1. We show that exposure of leukemia cells to daunorubicin activated an integrated stress response-like transcriptional program to induce ABCB1 through remodeling and activation of an ATF4-bound, stress-responsive enhancer. Protracted stress primed enhancers for rapid increases in activity following re-exposure of cells to daunorubicin, providing an epigenetic memory of prior drug treatment. In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-responsive enhancer and led to dose-dependent induction of ABCB1. Dynamic induction of ABCB1 by diverse stressors, including chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhibition, providing an explanation for the failure of ABCB1 inhibitors in clinical trials. Stress-induced up regulation of ABCB1 was mitigated by combined use of pharmacologic inhibitors U0126 and ISRIB, which inhibit stress signalling and have potential for use as adjuvants to enhance the activity of ABCB1 inhibitors.</p>',
			'date' => '2019-11-26',
			'pmid' => 'http://www.pubmed.gov/31770110',
			'doi' => '/',
			'modified' => '2020-02-25 13:46:19',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3764',
			'name' => 'The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress.',
			'authors' => 'Moreno Leon L, Gautier M, Allan R, Ilié M, Nottet N, Pons N, Paquet A, Lebrigand K, Truchi M, Fassy J, Magnone V, Kinnebrew G, Radovich M, Cheok MH, Barbry P, Vassaux G, Marquette CH, Ponzio G, Ivan M, Pottier N, Hofman P, Mari B, Rezzonico R',
			'description' => '<p>Lung cancer is the leading cause of cancer death worldwide, with poor prognosis and a high rate of recurrence despite early surgical removal. Hypoxic regions within tumors represent sources of aggressiveness and resistance to therapy. Although long non-coding RNAs (lncRNAs) are increasingly recognized as major gene expression regulators, their regulation and function following hypoxic stress are still largely unexplored. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-&kappa;B and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.</p>',
			'date' => '2019-08-15',
			'pmid' => 'http://www.pubmed.gov/31417181',
			'doi' => '10.1038/s41388-019-0935-y',
			'modified' => '2019-10-03 10:00:42',
			'created' => '2019-10-02 16:16:55',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '3690',
			'name' => 'P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.',
			'authors' => 'Bugai A, Quaresma AJC, Friedel CC, Lenasi T, Düster R, Sibley CR, Fujinaga K, Kukanja P, Hennig T, Blasius M, Geyer M, Ule J, Dölken L, Barborič M',
			'description' => '<p>DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain ill defined. Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nuclear ribonucleoprotein (7SK snRNP). This is mediated by activation of p38, which triggers enhanced binding of RBM7 with core subunits of 7SK snRNP. In turn, P-TEFb relocates to chromatin to induce transcription of short units, including key DDR genes and multiple classes of non-coding RNAs. Critically, interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-inducing agents due to activation of apoptosis. Our work uncovers the importance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival transcriptional response that is crucial for cell fate upon genotoxic insult.</p>',
			'date' => '2019-04-18',
			'pmid' => 'http://www.pubmed.gov/30824372',
			'doi' => '10.1016/j.molcel.2019.01.033',
			'modified' => '2019-06-28 13:53:03',
			'created' => '2019-06-21 14:55:31',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3597',
			'name' => 'The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.',
			'authors' => 'Tsuda M, Fukuda A, Roy N, Hiramatsu Y, Leonhardt L, Kakiuchi N, Hoyer K, Ogawa S, Goto N, Ikuta K, Kimura Y, Matsumoto Y, Takada Y, Yoshioka T, Maruno T, Yamaga Y, Kim GE, Akiyama H, Ogawa S, Wright CV, Saur D, Takaori K, Uemoto S, Hebrok M, Chiba T, Seno',
			'description' => '<p>Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.</p>',
			'date' => '2018-08-01',
			'pmid' => 'http://www.pubmed.gov/30010625',
			'doi' => '10.1172/JCI94287.',
			'modified' => '2019-04-17 15:09:09',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '3589',
			'name' => 'A new metabolic gene signature in prostate cancer regulated by JMJD3 and EZH2.',
			'authors' => 'Daures M, Idrissou M, Judes G, Rifaï K, Penault-Llorca F, Bignon YJ, Guy L, Bernard-Gallon D',
			'description' => '<p>Histone methylation is essential for gene expression control. Trimethylated lysine 27 of histone 3 (H3K27me3) is controlled by the balance between the activities of JMJD3 demethylase and EZH2 methyltransferase. This epigenetic mark has been shown to be deregulated in prostate cancer, and evidence shows H3K27me3 enrichment on gene promoters in prostate cancer. To study the impact of this enrichment, a transcriptomic analysis with TaqMan Low Density Array (TLDA) of several genes was studied on prostate biopsies divided into three clinical grades: normal ( = 23) and two tumor groups that differed in their aggressiveness (Gleason score &le; 7 ( = 20) and &gt;7 ( = 19)). ANOVA demonstrated that expression of the gene set was upregulated in tumors and correlated with Gleason score, thus discriminating between the three clinical groups. Six genes involved in key cellular processes stood out: , , , , and . Chromatin immunoprecipitation demonstrated collocation of EZH2 and JMJD3 on gene promoters that was dependent on disease stage. Gene set expression was also evaluated on prostate cancer cell lines (DU 145, PC-3 and LNCaP) treated with an inhibitor of JMJD3 (GSK-J4) or EZH2 (DZNeP) to study their involvement in gene regulation. Results showed a difference in GSK-J4 sensitivity under PTEN status of cell lines and an opposite gene expression profile according to androgen status of cells. In summary, our data describe the impacts of JMJD3 and EZH2 on a new gene signature involved in prostate cancer that may help identify diagnostic and therapeutic targets in prostate cancer.</p>',
			'date' => '2018-05-04',
			'pmid' => 'http://www.pubmed.gov/29805743',
			'doi' => '10.18632/oncotarget.25182',
			'modified' => '2019-04-17 15:21:33',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '3272',
			'name' => 'SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription',
			'authors' => 'Tran N.T. et al.',
			'description' => '<p>The structural maintenance of chromosomes (SMC) complex plays an important role in chromosome organization and segregation in most living organisms. In Caulobacter crescentus, SMC is required to align the left and the right arms of the chromosome that run in parallel down the long axis of the cell. However,&nbsp;the mechanism of SMC-mediated alignment of chromosomal arms remains elusive. Here, using genome-wide methods and microscopy of single cells, we show that Caulobacter SMC is recruited to the centromeric parS site and that SMC-mediated arm alignment depends on the chromosome-partitioning protein ParB. We provide evidence that SMC likely tethers the parS-proximal regions of the chromosomal arms together, promoting arm alignment. Furthermore, we show that highly transcribed genes near parS that are oriented against SMC translocation disrupt arm alignment, suggesting that head-on transcription interferes with SMC translocation. Our results demonstrate a tight interdependence of bacterial chromosome organization and global patterns of transcription.</p>',
			'date' => '2017-08-29',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28854358',
			'doi' => '',
			'modified' => '2017-10-16 09:48:59',
			'created' => '2017-10-16 09:48:59',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '3105',
			'name' => 'EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells',
			'authors' => 'Beringer M. et al.',
			'description' => '<p>The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding factor at the promoters of bivalent sites. Biochemical and genome-wide analyses show that Elongin BC is associated with Polycomb Repressive Complex 2 (PRC2) in pluripotent stem cells. Elongin BC is recruited to chromatin by the PRC2-associated&nbsp;factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein, also termed C17orf96, esPRC2p48, E130012A19Rik), a protein expressed in the inner cell mass of the mouse blastocyst. Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. Our results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.</p>',
			'date' => '2016-11-17',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27863225',
			'doi' => '',
			'modified' => '2017-01-03 16:02:21',
			'created' => '2017-01-03 16:02:21',
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	(int) 8 => 'NL',
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            <h6 style="height:60px">iDeal ChIP-seq kit for Transcription Factors</h6>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
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<tbody>
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<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
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<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
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<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
<p></p>',
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
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<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
	'label2' => 'Species, cell lines, tissues tested',
	'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
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	'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
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<tbody>
<tr>
<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
</tr>
<tr>
<td style="width: 144px;">Cells</td>
<td style="width: 267px; text-align: center;"><strong>4,000,000</strong></td>
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<tr>
<td style="width: 144px;">Tissues</td>
<td style="width: 267px; text-align: center;"><strong>30 mg</strong></td>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
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<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
			'label2' => 'Species, cell lines, tissues tested',
			'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
			'label3' => 'Additional solutions compatible with iDeal ChIP-seq kit for Transcription Factors',
			'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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<div class="small-12 medium-12 large-12 columns text-justify">
<p class="text-justify">Chromatin Immunoprecipitation (ChIP) coupled with quantitative PCR can be used to investigate protein-DNA interaction at known genomic binding sites. if sites are not known, qPCR primers can also be designed against potential regulatory regions such as promoters. ChIP-qPCR is advantageous in studies that focus on specific genes and potential regulatory regions across differing experimental conditions as the cost of performing real-time PCR is minimal. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</p>
<p class="text-justify"><strong>The ChIP-qPCR workflow</strong></p>
</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /> <img src="https://www.diagenode.com/img/chip-qpcr-diagram.png" /></div>
<div class="small-12 medium-12 large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>cell fixation (cross-linking) of chromatin-bound proteins such as histones or transcription factors to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing: </strong>fragmentation of chromatin<strong> </strong>by sonication down to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: protein-DNA complexe capture using<strong> <a href="https://www.diagenode.com/en/categories/chip-grade-antibodies">specific ChIP-grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: chromatin reverse cross-linking and elution followed by purification<strong> </strong></li>
<li class="large-12 columns"><strong>qPCR and analysis</strong>: using previously designed primers to amplify IP'd material at specific loci</li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/which-kit-to-choose"><img src="https://www.diagenode.com/img/banners/banner-decide.png" alt="" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="https://www.diagenode.com/pages/chip-kit-customizer-1"><img src="https://www.diagenode.com/img/banners/banner-customizer.png" alt="" /></a></div>
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			'description' => '<div class="row">
<div class="large-12 columns">Chromatin Immunoprecipitation (ChIP) coupled with high-throughput massively parallel sequencing as a detection method (ChIP-seq) has become one of the primary methods for epigenomics researchers, namely to investigate protein-DNA interaction on a genome-wide scale. This technique is now used in a variety of life science disciplines including cellular differentiation, tumor suppressor gene silencing, and the effect of histone modifications on gene expression.</div>
<div class="large-12 columns"></div>
<h5 class="large-12 columns"><strong></strong></h5>
<h5 class="large-12 columns"><strong>The ChIP-seq workflow</strong></h5>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/chip-seq-diagram.png" /></div>
<div class="large-12 columns"><br />
<ol>
<li class="large-12 columns"><strong>Chromatin preparation: </strong>Crosslink&nbsp;chromatin-bound proteins (histones or transcription factors) to DNA followed by cell lysis.</li>
<li class="large-12 columns"><strong>Chromatin shearing:</strong> Fragment chromatin by&nbsp;sonication to desired fragment size (100-500 bp)</li>
<li class="large-12 columns"><strong>Chromatin IP</strong>: Capture protein-DNA complexes with&nbsp;<strong><a href="../categories/chip-seq-grade-antibodies">specific ChIP-seq grade antibodies</a></strong>&nbsp;against the histone or transcription factor of interest</li>
<li class="large-12 columns"><strong>DNA purification</strong>: Reverse&nbsp;cross-links, elute, and purify&nbsp;</li>
<li class="large-12 columns"><strong>NGS Library Preparation</strong>: Ligate adapters and amplify&nbsp;IP'd material</li>
<li class="large-12 columns"><strong>Bioinformatic analysis</strong>: Perform r<span style="font-weight: 400;">ead filtering and trimming</span>, r<span style="font-weight: 400;">ead specific alignment, enrichment specific peak calling, QC metrics, multi-sample cross-comparison etc. </span></li>
</ol>
</div>
</div>
<div class="row" style="margin-top: 32px;">
<div class="small-12 medium-10 large-9 small-centered columns">
<div class="radius panel" style="background-color: #fff;">
<h3 class="text-center" style="color: #b21329;">Need guidance?</h3>
<p class="text-justify">Choose our full ChIP kits or simply choose what you need from antibodies, buffers, beads, chromatin shearing and purification reagents. With the ChIP Kit Customizer, you have complete flexibility on which components you want from our validated ChIP kits.</p>
<div class="row">
<div class="small-6 medium-6 large-6 columns"><a href="../pages/which-kit-to-choose"><img alt="" src="https://www.diagenode.com/img/banners/banner-decide.png" /></a></div>
<div class="small-6 medium-6 large-6 columns"><a href="../pages/chip-kit-customizer-1"><img alt="" src="https://www.diagenode.com/img/banners/banner-customizer.png" /></a></div>
</div>
</div>
</div>
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			'meta_description' => 'Diagenode offers wide range of kits and antibodies for Chromatin Immunoprecipitation Sequencing (ChIP-Seq) and also provides Bioruptor for chromatin shearing',
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<div class="small-12 medium-12 large-12 columns">The most important steps for a successful ChIP include both cell fixation and lysis, and chromatin shearing. Researchers often overlook the critical nature of both of these steps. Eliminating inconsistencies in the shearing step, <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> uses state-of-the-art ultrasound <strong>ACT</strong> (<strong>A</strong>daptive <strong>C</strong>avitation <strong>T</strong>echnology) to efficiently shear chromatin. ACT enables the highest chromatin quality for high IP efficiency and sensitivity for ChIP experiments with gentle yet highly effective shearing forces. Additionally, the Bioruptor<sup>&reg;</sup> provides a precisely controlled temperature environment that preserves chromatin from heat degradation such that protein-DNA complexes are well-preserved for sensitive, unbiased, and accurate ChIP.<br /><br /> <strong>Diagenode's Bioruptor</strong><sup>&reg;</sup> is the instrument of choice for chromatin shearing used for a number of downstream applications such as qPCR and ChIP-seq that require optimally sheared, unbiased chromatin.</div>
<div class="small-12 medium-12 large-12 columns text-center"><br /><img src="https://www.diagenode.com/img/applications/pico_dna_shearing_fig2.png" /></div>
<div class="small-10 medium-10 large-10 columns end small-offset-1"><small> <br /><strong>Panel A, 10 &micro;l volume:</strong> Chromatin samples are sheared for 10, 20 and 30 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.1 ml Bioruptor&reg; Microtubes (Cat. No. B01200041). <strong>Panel B, 100 &micro;l volume:</strong> Chromatin samples are sheared for 10 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using 0.65 ml Bioruptor&reg; Microtubes (Cat. No. WA-005-0500). <strong>Panel C, 300 &micro;l volume:</strong> Chromatin samples are sheared for 5, 10 and 15 cycles of 30 sec ON/30 sec OFF with the Bioruptor&reg; Pico using using 1.5 ml Bioruptor microtubes (Cat. No. C30010016).&nbsp;Prior to de-crosslinking, samples are treated with RNase cocktail mixture at 37&deg;C during 1 hour. The sheared chromatin is then de-crosslinked overnight and phenol/chloroform purified as described in the kit manual. 10 &micro;l of DNA (equivalent of 500, 000 cells) are analyzed on a 2% agarose gel (MW corresponds to the 100 bp DNA molecular weight marker).</small></div>
<div class="small-12 medium-12 large-12 columns"><br /><br /></div>
<div class="small-12 medium-12 large-12 columns">
<p>It is important to establish optimal conditions to shear crosslinked chromatin to get the correct fragment sizes needed for ChIP. Usually this process requires both optimizing sonication conditions as well as optimizing SDS concentration, which is laborious. With the Chromatin Shearing Optimization Kits, optimization is fast and easy - we provide optimization reagents with varying concentrations of SDS. Moreover, our Chromatin Shearing Optimization Kits can be used for the optimization of chromatin preparation with our kits for ChIP.</p>
</div>
<div class="small-12 medium-12 large-12 columns">
<div class="page" title="Page 7">
<table>
<tbody>
<tr valign="middle">
<td></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-100-million-cells">Chromatin Shearing Kit Low SDS (for Histone)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns">Chromatin Shearing Kit Low SDS (for TF)</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-high-sds-100-million-cells">Chromatin Shearing Kit High SDS</a></strong></td>
<td style="text-align: center;"><strong><a href="https://www.diagenode.com/p/chromatin-shearing-optimization-kit-medium-sds-100-million-cells">Chromatin Shearing Kit (for Plant)</a></strong></td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>SDS concentration</strong></p>
</td>
<td style="text-align: center;">
<p>&lt; 0.1%</p>
</td>
<td style="text-align: center;">
<p>0.2%</p>
</td>
<td style="text-align: center;">
<p>1%</p>
</td>
<td style="text-align: center;">
<p>0.5%</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Nuclei isolation</strong></p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
<td style="text-align: center;">
<p>No</p>
</td>
<td style="text-align: center;">
<p>Yes</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Allows for shearing of... cells/tissue</strong></p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>100 million cells</p>
</td>
<td style="text-align: center;">
<p>up to 25 g of tissue</p>
</td>
</tr>
<tr valign="middle" style="background-color: #fff;">
<td>
<p><strong>Corresponding to shearing buffers from</strong></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-x24-24-rxns">iDeal ChIP-seq kit for Histones</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">iDeal ChIP-seq Kit for Transcription Factors</a></p>
<p><a href="https://www.diagenode.com/en/p/ideal-chip-qpcr-kit">iDeal ChIP qPCR kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/true-microchip-kit-x16-16-rxns">True MicroChIP kit</a></p>
</td>
<td style="text-align: center;">
<p><a href="https://www.diagenode.com/en/p/universal-plant-chip-seq-kit-x24-24-rxns">Universal Plant ChIP-seq kit</a></p>
</td>
</tr>
</tbody>
</table>
<p><em><span style="font-weight: 400;">Table comes from our </span><a href="https://www.diagenode.com/protocols/bioruptor-pico-chromatin-preparation-guide"><span style="font-weight: 400;">Guide for successful chromatin preparation using the Bioruptor&reg; Pico</span></a></em></p>
</div>
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			'meta_title' => 'Chromatin shearing using Bioruptor® sonication device | Diagenode',
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			'name' => 'エピジェネティクス・クロマチン解析',
			'description' => '<div class="row">
<div class="large-12 columns">エピジェネティクス研究は、異なる転写パターン、遺伝子発現およびサイレンシングを引き起こすクロマチンの変化に対処します。<br /><br />クロマチンの主成分はDNA<span>およびヒストン蛋白質です。<span>&nbsp;</span></span>各ヒストンコア蛋白質（H2A<span>、</span>H2B<span>、</span>H3<span>および</span>H4<span>）の</span>2<span>つのコピーを</span>8<span>量体に組み込み、</span>DNA<span>で包んでヌクレオソームコアを形成させます。<span>&nbsp;</span></span>ヌクレオソームは、転写機械のDNA<span>への接近可能性および</span>クロマチン再構成因子を制御します。</div>
<div class="large-12 columns">
<p></p>
<p>クロマチン免疫沈降（ChIP<span>）は、関心対象の特定の蛋白質に対するゲノム結合部位の位置を解明するために使用される方法であり、遺伝子発現の制御に関する非常に貴重な洞察を提供します。<span>&nbsp;</span></span>ChIPは特定の抗原を含むクロマチン断片の選択的富化に関与します。 特定の蛋白質または蛋白質修飾を認識する抗体を使用して、特定の遺伝子座における抗原の相対存在量を決定します。</p>
<p>ChIP-seq<span>および</span>ChIP-qPCR<span>は、蛋白質</span>-DNA<span>結合部位の同定を可能にする技術です。</span></p>
<p>&nbsp;</p>
</div>
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<p><span>The first step of a ChIP assay is the cross-linking in order to fix the cells. Cross-linking is typically achieved by using formaldehyde which forms reversible DNA-protein links. Formaldehyde rapidly permeates the cell membranes and enables a fast cross-linking of closely associated proteins in intact cells. However, formaldehyde is usually not effective to cross-link proteins that are not directly bound to the DNA. For example, chromatin interactions with inducible transcription factors or with cofactors that interact with DNA through protein-protein interactions are not well preserve with formaldehyde. So, for higher order and/or dynamic interactions, other cross-linkers should be considered for efficient protein-protein stabilization such as the Diagenode ChIP cross-link Gold. This reagent is to use in combination with formaldehyde. The protocol involves a sequential fixation. A first protein-protein fixation by the ChIP cross-link Gold followed by protein-DNA fixation by formaldehyde. </span></p>
<p><span>Format: </span><span>supplied as a 250 x concentrated solution<br /> </span><span>Shipping conditions</span><span>: shipped at -20&deg;C<br /> </span><span>Storage conditions</span><span>: Store at -20&deg;C; for long storage, store at -80&deg;C. Avoid multiple freeze-thaw cycles. </span></p>
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			'name' => 'Chromatin shearing - Guide for successful chromatin preparation using the Bioruptor<sup>&reg;</sup> Pico',
			'description' => '<p><span>Chromatin immunoprecipitation (ChIP) is a common tool used to study protein-DNA interactions in cells and tissues. The assay can be cumbersome and the success is highly dependent on the quality of chromatin. The first critical step of a successful ChIP experiment is the preparation of sheared chromatin which is representative of the biological scenario of interest. </span></p>',
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			'name' => 'Differentiation block in acute myeloid leukemia regulated by intronicsequences of FTO',
			'authors' => 'Camera  F. et al.',
			'description' => '<p>Iroquois transcription factor gene IRX3 is highly expressed in 20&acirc;&euro;&ldquo;30\% of acute myeloid leukemia (AML) and contributes to the pathognomonic differentiation block. Intron 8 FTO sequences &acirc;&circ;&frac14;220kB downstream of IRX3 exhibit histone acetylation, DNA methylation, and contacts with the IRX3 promoter, which correlate with IRX3 expression. Deletion of these intronic elements confirms a role in positively regulating IRX3. RNAseq revealed long non-coding (lnc) transcripts arising from this locus. FTO-lncAML knockdown (KD) induced differentiation of AML cells, loss of clonogenic activity, and reduced FTO intron 8:IRX3 promoter contacts. While both FTO-lncAML KD and IRX3 KD induced differentiation, FTO-lncAML but not IRX3 KD led to HOXA downregulation suggesting transcript activity in trans. FTO-lncAMLhigh AML samples expressed higher levels of HOXA and lower levels of differentiation genes. Thus, a regulatory module in FTO intron 8 consisting of clustered enhancer elements and a long non-coding RNA is active in human AML, impeding myeloid differentiation.</p>',
			'date' => '2023-08-01',
			'pmid' => 'https://www.sciencedirect.com/science/article/pii/S2589004223013962',
			'doi' => '10.1016/j.isci.2023.107319',
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			'description' => '<p><span>Skin aging is characterized by structural and functional changes that contribute to age-associated frailty. This probably depends on synergy between alterations in the local niche and stem cell-intrinsic changes, underscored by proinflammatory microenvironments that drive pleotropic changes. The nature of these age-associated inflammatory cues, or how they affect tissue aging, is unknown. Based on single-cell RNA sequencing of the dermal compartment of mouse skin, we show a skew towards an IL-17-expressing phenotype of T helper cells, &gamma;&delta; T cells and innate lymphoid cells in aged skin. Importantly, in vivo blockade of IL-17 signaling during aging reduces the proinflammatory state of the skin, delaying the appearance of age-related traits. Mechanistically, aberrant IL-17 signals through NF-&kappa;B in epidermal cells to impair homeostatic functions while promoting an inflammatory state. Our results indicate that aged skin shows signs of chronic inflammation and that increased IL-17 signaling could be targeted to prevent age-associated skin ailments.</span></p>',
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			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/37291218',
			'doi' => '10.1038/s43587-023-00431-z',
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			'authors' => 'Tzeplaeff  L. et al.',
			'description' => '<p>Cytoplasmic mislocalization of the nuclear Fused in Sarcoma (FUS) protein is associated to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Cytoplasmic FUS accumulation is recapitulated in the frontal cortex and spinal cord of heterozygous Fus mice. Yet, the mechanisms linking FUS mislocalization to hippocampal function and memory formation are still not characterized. Herein, we show that in these mice, the hippocampus paradoxically displays nuclear FUS accumulation. Multi-omic analyses showed that FUS binds to a set of genes characterized by the presence of an ETS/ELK-binding motifs, and involved in RNA metabolism, transcription, ribosome/mitochondria and chromatin organization. Importantly, hippocampal nuclei showed a decompaction of the neuronal chromatin at highly expressed genes and an inappropriate transcriptomic response was observed after spatial training of Fus mice. Furthermore, these mice lacked precision in a hippocampal-dependent spatial memory task and displayed decreased dendritic spine density. These studies shows that mutated FUS affects epigenetic regulation of the chromatin landscape in hippocampal neurons, which could participate in FTD/ALS pathogenic events. These data call for further investigation in the neurological phenotype of FUS-related diseases and open therapeutic strategies towards epigenetic drugs.</p>',
			'date' => '2023-06-01',
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			'description' => '<p>In addition to its role in chromosome maintenance, the six-membered Smc5/6 complex functions as a restriction factor that binds to and transcriptionally silences viral and other episomal DNA. However, the underlying mechanism is unknown. Here, we show that transcriptional silencing by the human Smc5/6 complex is a three-step process. The first step is entrapment of the episomal DNA by a mechanism dependent on Smc5/6 ATPase activity and a function of its Nse4a subunit for which the Nse4b paralog cannot substitute. The second step results in Smc5/6 recruitment to promyelocytic leukemia nuclear bodies by SLF2 (the human ortholog of Nse6). The third step promotes silencing through a mechanism requiring Nse2 but not its SUMO ligase activity. By contrast, the related cohesin and condensin complexes fail to bind to or silence episomal DNA, indicating a property unique to Smc5/6.</p>',
			'date' => '2022-09-01',
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			'doi' => '10.1038/s41594-022-00829-0',
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			'name' => 'Androgen-Induced MIG6 Regulates Phosphorylation ofRetinoblastoma Protein and AKT to Counteract Non-Genomic ARSignaling in Prostate Cancer Cells.',
			'authors' => 'Schomann  T. et al.',
			'description' => '<p>The bipolar androgen therapy (BAT) includes the treatment of prostate cancer (PCa) patients with supraphysiological androgen level (SAL). Interestingly, SAL induces cell senescence in PCa cell lines as well as ex vivo in tumor samples of patients. The SAL-mediated cell senescence was shown to be androgen receptor (AR)-dependent and mediated in part by non-genomic AKT signaling. RNA-seq analyses compared with and without SAL treatment as well as by AKT inhibition (AKTi) revealed a specific transcriptome landscape. Comparing the top 100 genes similarly regulated by SAL in two human PCa cell lines that undergo cell senescence and being counteracted by AKTi revealed 33 commonly regulated genes. One gene, ERBB receptor feedback inhibitor 1 (), encodes the mitogen-inducible gene 6 (MIG6) that is potently upregulated by SAL, whereas the combinatory treatment of SAL with AKTi reverses the SAL-mediated upregulation. Functionally, knockdown of enhances the pro-survival AKT pathway by enhancing phosphorylation of AKT and the downstream AKT target S6, whereas the phospho-retinoblastoma (pRb) protein levels were decreased. Further, the expression of the cell cycle inhibitor p15 is enhanced by SAL and knockdown. In line with this, cell senescence is induced by knockdown and is enhanced slightly further by SAL. Treatment of SAL in the knockdown background enhances phosphorylation of both AKT and S6 whereas pRb becomes hypophosphorylated. Interestingly, the knockdown does not reduce AR protein levels or AR target gene expression, suggesting that MIG6 does not interfere with genomic signaling of AR but represses androgen-induced cell senescence and might therefore counteract SAL-induced signaling. The findings indicate that SAL treatment, used in BAT, upregulates MIG6, which inactivates both pRb and the pro-survival AKT signaling. This indicates a novel negative feedback loop integrating genomic and non-genomic AR signaling.</p>',
			'date' => '2022-07-01',
			'pmid' => 'https://doi.org/10.3390%2Fbiom12081048',
			'doi' => '10.3390/biom12081048',
			'modified' => '2022-10-21 09:33:25',
			'created' => '2022-09-28 09:53:13',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 5 => array(
			'id' => '4240',
			'name' => 'Soluble guanylate cyclase signalling mediates etoposide resistance inprogressing small cell lung cancer',
			'authors' => 'Schenk MW et al. ',
			'description' => '<p>Small cell lung cancer (SCLC) has a 5-year survival rate of \&lt;7\%. Rapid emergence of acquired resistance to standard platinum-etoposide chemotherapy is common and improved therapies are required for this recalcitrant tumour. We exploit six paired pre-treatment and post-chemotherapy circulating tumour cell patient-derived explant (CDX) models from donors with extensive stage SCLC to investigate changes at disease progression after chemotherapy. Soluble guanylate cyclase (sGC) is recurrently upregulated in post-chemotherapy progression CDX models, which correlates with acquired chemoresistance. Expression and activation of sGC is regulated by Notch and nitric oxide (NO) signalling with downstream activation of protein kinase G. Genetic targeting of sGC or pharmacological inhibition of NO synthase re-sensitizes a chemoresistant CDX progression model in vivo, revealing this pathway as a mediator of chemoresistance and potential vulnerability of relapsed SCLC.</p>',
			'date' => '2021-11-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/34789728',
			'doi' => '10.1038/s41467-021-26823-6',
			'modified' => '2022-05-19 17:11:56',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 6 => array(
			'id' => '4319',
			'name' => 'Regulatory interplay between Vav1, Syk and β-catenin occurs in lungcancer cells.',
			'authors' => 'Boudria Rofia et al. ',
			'description' => '<p>Vav1 exhibits two signal transducing properties as an adaptor protein and a regulator of cytoskeleton organization through its Guanine nucleotide Exchange Factor module. Although the expression of Vav1 is restricted to the hematopoietic lineage, its ectopic expression has been unraveled in a number of solid tumors. In this study, we show that in lung cancer cells, as such in hematopoietic cells, Vav1 interacts with the Spleen Tyrosine Kinase, Syk. Likewise, Syk interacts with &beta;-catenin and, together with Vav1, regulates the phosphorylation status of &beta;-catenin. Depletion of Vav1, Syk or &beta;-catenin inhibits Rac1 activity and decreases cell migration suggesting the interplay of the three effectors to a common signaling pathway. This model is further supported by the finding that in turn, &beta;-catenin regulates the transcription of Syk gene expression. This study highlights the elaborated connection between Vav1, Syk and &beta;-catenin and the contribution of the trio to cell migration.</p>',
			'date' => '2021-10-01',
			'pmid' => 'https://doi.org/10.1016%2Fj.cellsig.2021.110079',
			'doi' => '10.1016/j.cellsig.2021.110079',
			'modified' => '2022-06-20 09:32:21',
			'created' => '2022-05-19 10:41:50',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 7 => array(
			'id' => '4171',
			'name' => 'Androgen receptor positively regulates gonadotropin-releasing hormonereceptor in pituitary gonadotropes.',
			'authors' => 'Ryan, Genevieve E. et al.',
			'description' => '<p>Within pituitary gonadotropes, the gonadotropin-releasing hormone receptor (GnRHR) receives hypothalamic input from GnRH neurons that is critical for reproduction. Previous studies have suggested that androgens may regulate GnRHR, although the mechanisms remain unknown. In this study, we demonstrated that androgens positively regulate Gnrhr mRNA in mice. We then investigated the effects of androgens and androgen receptor (AR) on Gnrhr promoter activity in immortalized mouse L&beta;T2 cells, which represent mature gonadotropes. We found that AR positively regulates the Gnrhr proximal promoter, and that this effect requires a hormone response element (HRE) half site at -159/-153 relative to the transcription start site. We also identified nonconsensus, full-length HREs at -499/-484 and -159/-144, which are both positively regulated by androgens on a heterologous promoter. Furthermore, AR associates with the Gnrhr promoter in ChIP. Altogether, we report that GnRHR is positively regulated by androgens through recruitment of AR to the Gnrhr proximal promoter.</p>',
			'date' => '2021-04-01',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/33872733',
			'doi' => '10.1016/j.mce.2021.111286',
			'modified' => '2021-12-21 15:57:35',
			'created' => '2021-12-06 15:53:19',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 8 => array(
			'id' => '4108',
			'name' => 'BAF complexes drive proliferation and block myogenic differentiation in fusion-positive rhabdomyosarcoma',
			'authors' => 'Laubscher et. al.',
			'description' => '<p><span>Rhabdomyosarcoma (RMS) is a pediatric malignancy of skeletal muscle lineage. The aggressive alveolar subtype is characterized by t(2;13) or t(1;13) translocations encoding for PAX3- or PAX7-FOXO1 chimeric transcription factors, respectively, and are referred to as fusion positive RMS (FP-RMS). The fusion gene alters the myogenic program and maintains the proliferative state wile blocking terminal differentiation. Here we investigated the contributions of chromatin regulatory complexes to FP-RMS tumor maintenance. We define, for the first time, the mSWI/SNF repertoire in FP-RMS. We find that&nbsp;</span><em>SMARCA4</em><span><span>&nbsp;</span>(encoding BRG1) is overexpressed in this malignancy compared to skeletal muscle and is essential for cell proliferation. Proteomic studies suggest proximity between PAX3-FOXO1 and BAF complexes, which is further supported by genome-wide binding profiles revealing enhancer colocalization of BAF with core regulatory transcription factors. Further, mSWI/SNF complexes act as sensors of chromatin state and are recruited to sites of<span>&nbsp;</span></span><em>de novo</em><span><span>&nbsp;</span>histone acetylation. Phenotypically, interference with mSWI/SNF complex function induces transcriptional activation of the skeletal muscle differentiation program associated with MYCN enhancer invasion at myogenic target genes which is reproduced by BRG1 targeting compounds. We conclude that inhibition of BRG1 overcomes the differentiation blockade of FP-RMS cells and may provide a therapeutic strategy for this lethal childhood tumor.</span></p>',
			'date' => '2021-01-07',
			'pmid' => 'https://www.researchsquare.com/article/rs-131009/v1',
			'doi' => ' 10.21203/rs.3.rs-131009/v1',
			'modified' => '2021-07-07 11:52:23',
			'created' => '2021-07-07 06:38:34',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 9 => array(
			'id' => '3997',
			'name' => 'The Human Integrator Complex Facilitates Transcriptional Elongation by Endonucleolytic Cleavage of Nascent Transcripts.',
			'authors' => 'Beckedorff F, Blumenthal E, daSilva LF, Aoi Y, Cingaram PR, Yue J, Zhang A, Dokaneheifard S, Valencia MG, Gaidosh G, Shilatifard A, Shiekhattar R',
			'description' => '<p>Transcription by RNA polymerase II (RNAPII) is pervasive in the human genome. However, the mechanisms controlling transcription at promoters and enhancers remain enigmatic. Here, we demonstrate that Integrator subunit 11 (INTS11), the catalytic subunit of the Integrator complex, regulates transcription at these loci through its endonuclease activity. Promoters of genes require INTS11 to cleave nascent transcripts associated with paused RNAPII and induce their premature termination in the proximity of the&nbsp;+1 nucleosome. The turnover of RNAPII permits the subsequent recruitment of an elongation-competent RNAPII complex, leading to productive elongation. In contrast, enhancers require INTS11 catalysis not to evict paused RNAPII but rather to terminate enhancer RNA transcription beyond the&nbsp;+1 nucleosome. These findings are supported by the differential occupancy of negative elongation factor (NELF), SPT5, and tyrosine-1-phosphorylated RNAPII. This study elucidates the role of Integrator in mediating transcriptional elongation at human promoters through the endonucleolytic cleavage of nascent transcripts and the dynamic turnover of RNAPII.</p>',
			'date' => '2020-07-21',
			'pmid' => 'http://www.pubmed.gov/32697989',
			'doi' => '10.1016/j.celrep.2020.107917',
			'modified' => '2020-09-01 14:44:33',
			'created' => '2020-08-21 16:41:39',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 10 => array(
			'id' => '3955',
			'name' => 'Inactivation of Arid1a in the endometrium is associated with endometrioid tumorigenesis through transcriptional reprogramming.',
			'authors' => 'Suryo Rahmanto Y, Shen W, Shi X, Chen X, Yu Y, Yu ZC, Miyamoto T, Lee MH, Singh V, Asaka R, Shimberg G, Vitolo MI, Martin SS, Wirtz D, Drapkin R, Xuan J, Wang TL, Shih IM',
			'description' => '<p>Somatic inactivating mutations of ARID1A, a SWI/SNF chromatin remodeling gene, are prevalent in human endometrium-related malignancies. To elucidate the mechanisms underlying how ARID1A deleterious mutation contributes to tumorigenesis, we establish genetically engineered murine models with Arid1a and/or Pten&nbsp;conditional deletion in the endometrium. Transcriptomic analyses on endometrial cancers and precursors derived from these mouse&nbsp;models show a close resemblance to human uterine endometrioid carcinomas. We identify transcriptional networks that are controlled by Arid1a and have an impact on endometrial tumor development. To verify findings from the murine models, we analyze ARID1A and ARID1A human endometrial epithelial cells. Using a system biology approach and functional studies, we demonstrate that ARID1A-deficiency lead to loss of TGF-&beta; tumor suppressive function and that inactivation of ARID1A/TGF-&beta; axis promotes migration and invasion of PTEN-deleted endometrial tumor cells. These findings provide molecular insights into how ARID1A inactivation accelerates endometrial tumor progression and dissemination, the major causes of cancer mortality.</p>',
			'date' => '2020-06-01',
			'pmid' => 'http://www.pubmed.gov/32483112',
			'doi' => '10.1038/s41467-020-16416-0',
			'modified' => '2020-08-17 09:18:26',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 11 => array(
			'id' => '3956',
			'name' => 'AP-1 controls the p11-dependent antidepressant response.',
			'authors' => 'Chottekalapanda RU, Kalik S, Gresack J, Ayala A, Gao M, Wang W, Meller S, Aly A, Schaefer A, Greengard P',
			'description' => '<p>Selective serotonin reuptake inhibitors (SSRIs) are the most widely prescribed drugs for mood disorders. While the mechanism of SSRI action is still unknown, SSRIs are thought to exert therapeutic effects by elevating extracellular serotonin levels in the brain, and remodel the structural and functional alterations dysregulated during depression. To determine their precise mode of action, we tested whether such neuroadaptive processes are modulated by regulation of specific gene expression programs. Here we identify a transcriptional program regulated by activator protein-1 (AP-1) complex, formed by c-Fos and c-Jun that is selectively activated prior to the onset of the chronic SSRI response. The AP-1 transcriptional program modulates the expression of key neuronal remodeling genes, including S100a10 (p11), linking neuronal plasticity to the antidepressant response. We find that AP-1 function is required for the antidepressant effect in vivo. Furthermore, we demonstrate how neurochemical pathways of BDNF and FGF2, through the MAPK, PI3K, and JNK cascades, regulate AP-1 function to mediate the beneficial effects of the antidepressant response. Here we put forth a sequential molecular network to track the antidepressant response and provide a new avenue that could be used to accelerate or potentiate antidepressant responses by triggering neuroplasticity.</p>',
			'date' => '2020-05-21',
			'pmid' => 'http://www.pubmed.gov/32439846',
			'doi' => '10.1038/s41380-020-0767-8',
			'modified' => '2020-08-17 09:17:39',
			'created' => '2020-08-10 12:12:25',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 12 => array(
			'id' => '3820',
			'name' => 'A stress-responsive enhancer induces dynamic drug resistance in acute myeloid leukemia.',
			'authors' => 'Williams MS, Amaral FM, Simeoni F, Somervaille TC',
			'description' => '<p>The drug efflux pump ABCB1 is a key driver of chemoresistance, and high expression predicts for treatment failure in acute myeloid leukemia (AML). In this study, we identified and functionally validated the network of enhancers that controls expression of ABCB1. We show that exposure of leukemia cells to daunorubicin activated an integrated stress response-like transcriptional program to induce ABCB1 through remodeling and activation of an ATF4-bound, stress-responsive enhancer. Protracted stress primed enhancers for rapid increases in activity following re-exposure of cells to daunorubicin, providing an epigenetic memory of prior drug treatment. In primary human AML, exposure of fresh blast cells to daunorubicin activated the stress-responsive enhancer and led to dose-dependent induction of ABCB1. Dynamic induction of ABCB1 by diverse stressors, including chemotherapy, facilitated escape of leukemia cells from targeted third-generation ABCB1 inhibition, providing an explanation for the failure of ABCB1 inhibitors in clinical trials. Stress-induced up regulation of ABCB1 was mitigated by combined use of pharmacologic inhibitors U0126 and ISRIB, which inhibit stress signalling and have potential for use as adjuvants to enhance the activity of ABCB1 inhibitors.</p>',
			'date' => '2019-11-26',
			'pmid' => 'http://www.pubmed.gov/31770110',
			'doi' => '/',
			'modified' => '2020-02-25 13:46:19',
			'created' => '2020-02-13 10:02:44',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 13 => array(
			'id' => '3764',
			'name' => 'The nuclear hypoxia-regulated NLUCAT1 long non-coding RNA contributes to an aggressive phenotype in lung adenocarcinoma through regulation of oxidative stress.',
			'authors' => 'Moreno Leon L, Gautier M, Allan R, Ilié M, Nottet N, Pons N, Paquet A, Lebrigand K, Truchi M, Fassy J, Magnone V, Kinnebrew G, Radovich M, Cheok MH, Barbry P, Vassaux G, Marquette CH, Ponzio G, Ivan M, Pottier N, Hofman P, Mari B, Rezzonico R',
			'description' => '<p>Lung cancer is the leading cause of cancer death worldwide, with poor prognosis and a high rate of recurrence despite early surgical removal. Hypoxic regions within tumors represent sources of aggressiveness and resistance to therapy. Although long non-coding RNAs (lncRNAs) are increasingly recognized as major gene expression regulators, their regulation and function following hypoxic stress are still largely unexplored. Combining profiling studies on early-stage lung adenocarcinoma (LUAD) biopsies and on A549 LUAD cell lines cultured in normoxic or hypoxic conditions, we identified a subset of lncRNAs that are both correlated with the hypoxic status of tumors and regulated by hypoxia in vitro. We focused on a new transcript, NLUCAT1, which is strongly upregulated by hypoxia in vitro and correlated with hypoxic markers and poor prognosis in LUADs. Full molecular characterization showed that NLUCAT1 is a large nuclear transcript composed of six exons and mainly regulated by NF-&kappa;B and NRF2 transcription factors. CRISPR-Cas9-mediated invalidation of NLUCAT1 revealed a decrease in proliferative and invasive properties, an increase in oxidative stress and a higher sensitivity to cisplatin-induced apoptosis. Transcriptome analysis of NLUCAT1-deficient cells showed repressed genes within the antioxidant and/or cisplatin-response networks. We demonstrated that the concomitant knockdown of four of these genes products, GPX2, GLRX, ALDH3A1, and PDK4, significantly increased ROS-dependent caspase activation, thus partially mimicking the consequences of NLUCAT1 inactivation in LUAD cells. Overall, we demonstrate that NLUCAT1 contributes to an aggressive phenotype in early-stage hypoxic tumors, suggesting it may represent a new potential therapeutic target in LUADs.</p>',
			'date' => '2019-08-15',
			'pmid' => 'http://www.pubmed.gov/31417181',
			'doi' => '10.1038/s41388-019-0935-y',
			'modified' => '2019-10-03 10:00:42',
			'created' => '2019-10-02 16:16:55',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 14 => array(
			'id' => '3690',
			'name' => 'P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress.',
			'authors' => 'Bugai A, Quaresma AJC, Friedel CC, Lenasi T, Düster R, Sibley CR, Fujinaga K, Kukanja P, Hennig T, Blasius M, Geyer M, Ule J, Dölken L, Barborič M',
			'description' => '<p>DNA damage response (DDR) involves dramatic transcriptional alterations, the mechanisms of which remain ill defined. Here, we show that following genotoxic stress, the RNA-binding motif protein 7 (RBM7) stimulates RNA polymerase II (Pol II) transcription and promotes cell viability by activating the positive transcription elongation factor b (P-TEFb) via its release from the inhibitory 7SK small nuclear ribonucleoprotein (7SK snRNP). This is mediated by activation of p38, which triggers enhanced binding of RBM7 with core subunits of 7SK snRNP. In turn, P-TEFb relocates to chromatin to induce transcription of short units, including key DDR genes and multiple classes of non-coding RNAs. Critically, interfering with the axis of RBM7 and P-TEFb provokes cellular hypersensitivity to DNA-damage-inducing agents due to activation of apoptosis. Our work uncovers the importance of stress-dependent stimulation of Pol II pause release, which enables a pro-survival transcriptional response that is crucial for cell fate upon genotoxic insult.</p>',
			'date' => '2019-04-18',
			'pmid' => 'http://www.pubmed.gov/30824372',
			'doi' => '10.1016/j.molcel.2019.01.033',
			'modified' => '2019-06-28 13:53:03',
			'created' => '2019-06-21 14:55:31',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 15 => array(
			'id' => '3597',
			'name' => 'The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis.',
			'authors' => 'Tsuda M, Fukuda A, Roy N, Hiramatsu Y, Leonhardt L, Kakiuchi N, Hoyer K, Ogawa S, Goto N, Ikuta K, Kimura Y, Matsumoto Y, Takada Y, Yoshioka T, Maruno T, Yamaga Y, Kim GE, Akiyama H, Ogawa S, Wright CV, Saur D, Takaori K, Uemoto S, Hebrok M, Chiba T, Seno',
			'description' => '<p>Chromatin remodeler Brahma related gene 1 (BRG1) is silenced in approximately 10% of human pancreatic ductal adenocarcinomas (PDAs). We previously showed that BRG1 inhibits the formation of intraductal pancreatic mucinous neoplasm (IPMN) and that IPMN-derived PDA originated from ductal cells. However, the role of BRG1 in pancreatic intraepithelial neoplasia-derived (PanIN-derived) PDA that originated from acinar cells remains elusive. Here, we found that exclusive elimination of Brg1 in acinar cells of Ptf1a-CreER; KrasG12D; Brg1fl/fl mice impaired the formation of acinar-to-ductal metaplasia (ADM) and PanIN independently of p53 mutation, while PDA formation was inhibited in the presence of p53 mutation. BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. SOX9 expression was downregulated in BRG1-depleted ADMs/PanINs. Notably, Sox9 overexpression canceled this PanIN-attenuated phenotype in KBC mice. Furthermore, Brg1 deletion in established PanIN by using a dual recombinase system resulted in regression of the lesions in mice. Finally, BRG1 expression correlated with SOX9 expression in human PDAs. In summary, BRG1 is critical for PanIN initiation and progression through positive regulation of SOX9. Thus, the BRG1/SOX9 axis is a potential target for PanIN-derived PDA.</p>',
			'date' => '2018-08-01',
			'pmid' => 'http://www.pubmed.gov/30010625',
			'doi' => '10.1172/JCI94287.',
			'modified' => '2019-04-17 15:09:09',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 16 => array(
			'id' => '3589',
			'name' => 'A new metabolic gene signature in prostate cancer regulated by JMJD3 and EZH2.',
			'authors' => 'Daures M, Idrissou M, Judes G, Rifaï K, Penault-Llorca F, Bignon YJ, Guy L, Bernard-Gallon D',
			'description' => '<p>Histone methylation is essential for gene expression control. Trimethylated lysine 27 of histone 3 (H3K27me3) is controlled by the balance between the activities of JMJD3 demethylase and EZH2 methyltransferase. This epigenetic mark has been shown to be deregulated in prostate cancer, and evidence shows H3K27me3 enrichment on gene promoters in prostate cancer. To study the impact of this enrichment, a transcriptomic analysis with TaqMan Low Density Array (TLDA) of several genes was studied on prostate biopsies divided into three clinical grades: normal ( = 23) and two tumor groups that differed in their aggressiveness (Gleason score &le; 7 ( = 20) and &gt;7 ( = 19)). ANOVA demonstrated that expression of the gene set was upregulated in tumors and correlated with Gleason score, thus discriminating between the three clinical groups. Six genes involved in key cellular processes stood out: , , , , and . Chromatin immunoprecipitation demonstrated collocation of EZH2 and JMJD3 on gene promoters that was dependent on disease stage. Gene set expression was also evaluated on prostate cancer cell lines (DU 145, PC-3 and LNCaP) treated with an inhibitor of JMJD3 (GSK-J4) or EZH2 (DZNeP) to study their involvement in gene regulation. Results showed a difference in GSK-J4 sensitivity under PTEN status of cell lines and an opposite gene expression profile according to androgen status of cells. In summary, our data describe the impacts of JMJD3 and EZH2 on a new gene signature involved in prostate cancer that may help identify diagnostic and therapeutic targets in prostate cancer.</p>',
			'date' => '2018-05-04',
			'pmid' => 'http://www.pubmed.gov/29805743',
			'doi' => '10.18632/oncotarget.25182',
			'modified' => '2019-04-17 15:21:33',
			'created' => '2019-04-16 12:25:30',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 17 => array(
			'id' => '3272',
			'name' => 'SMC Progressively Aligns Chromosomal Arms in Caulobacter crescentus but Is Antagonized by Convergent Transcription',
			'authors' => 'Tran N.T. et al.',
			'description' => '<p>The structural maintenance of chromosomes (SMC) complex plays an important role in chromosome organization and segregation in most living organisms. In Caulobacter crescentus, SMC is required to align the left and the right arms of the chromosome that run in parallel down the long axis of the cell. However,&nbsp;the mechanism of SMC-mediated alignment of chromosomal arms remains elusive. Here, using genome-wide methods and microscopy of single cells, we show that Caulobacter SMC is recruited to the centromeric parS site and that SMC-mediated arm alignment depends on the chromosome-partitioning protein ParB. We provide evidence that SMC likely tethers the parS-proximal regions of the chromosomal arms together, promoting arm alignment. Furthermore, we show that highly transcribed genes near parS that are oriented against SMC translocation disrupt arm alignment, suggesting that head-on transcription interferes with SMC translocation. Our results demonstrate a tight interdependence of bacterial chromosome organization and global patterns of transcription.</p>',
			'date' => '2017-08-29',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/28854358',
			'doi' => '',
			'modified' => '2017-10-16 09:48:59',
			'created' => '2017-10-16 09:48:59',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		),
		(int) 18 => array(
			'id' => '3105',
			'name' => 'EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells',
			'authors' => 'Beringer M. et al.',
			'description' => '<p>The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding factor at the promoters of bivalent sites. Biochemical and genome-wide analyses show that Elongin BC is associated with Polycomb Repressive Complex 2 (PRC2) in pluripotent stem cells. Elongin BC is recruited to chromatin by the PRC2-associated&nbsp;factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein, also termed C17orf96, esPRC2p48, E130012A19Rik), a protein expressed in the inner cell mass of the mouse blastocyst. Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. Our results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.</p>',
			'date' => '2016-11-17',
			'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27863225',
			'doi' => '',
			'modified' => '2017-01-03 16:02:21',
			'created' => '2017-01-03 16:02:21',
			'ProductsPublication' => array(
				[maximum depth reached]
			)
		)
	),
	'Testimonial' => array(),
	'Area' => array(),
	'SafetySheet' => array(
		(int) 0 => array(
			'id' => '2350',
			'name' => 'ChIP Cross-link Gold SDS GB en',
			'language' => 'en',
			'url' => 'files/SDS/ChIP_Cross-link/SDS-C01019027-ChIP_Cross-link_Gold-GB-en-GHS_1_0.pdf',
			'countries' => 'GB',
			'modified' => '2022-08-29 15:20:14',
			'created' => '2022-08-29 15:20:14',
			'ProductsSafetySheet' => array(
				[maximum depth reached]
			)
		),
		(int) 1 => array(
			'id' => '2352',
			'name' => 'ChIP Cross-link Gold SDS US en',
			'language' => 'en',
			'url' => 'files/SDS/ChIP_Cross-link/SDS-C01019027-ChIP_Cross-link_Gold-US-en-GHS_1_0.pdf',
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            <h6 style="height:60px">iDeal ChIP-seq kit for Transcription Factors</h6>
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<p><span style="font-weight: 400;">Diagenode&rsquo;s <strong>iDeal ChIP-seq Kit for Transcription Factors</strong> is a highly validated solution for robust transcription factor and other non-histone proteins ChIP-seq results and contains everything you need for start-to-finish </span><b>ChIP </b><span style="font-weight: 400;">prior to </span><b>Next-Generation Sequencing</b><span style="font-weight: 400;">. This complete solution contains all buffers and reagents for cell lysis, chromatin shearing, immunoprecipitation, and DNA purification. In addition, unlike competing solutions, the kit contains positive and negative control antibodies (CTCF and IgG, respectively) as well as positive and negative control PCR primers pairs (H19 and Myoglobin exon 2, respectively) for your convenience and a guarantee of optimal results. <br /></span></p>
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<p><span style="font-weight: 400;">The </span><b>&nbsp;iDeal ChIP-seq kit for Transcription Factors </b><span style="font-weight: 400;">is compatible for cells or tissues:</span></p>
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<td style="width: 144px;"></td>
<td style="width: 267px; text-align: center;"><span style="font-weight: 400;">Amount per IP</span></td>
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<td style="width: 144px;">Cells</td>
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<p><span style="font-weight: 400;">The iDeal ChIP-seq kit is the only kit on the market validated for major sequencing systems. Our expertise in ChIP-seq tools allows reproducible and efficient results every time. </span></p>
<p></p>
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<li><span style="font-weight: 400;"><strong>Highly optimized protocol</strong> for ChIP-seq from cells and tissues</span></li>
<li><span style="font-weight: 400;"><strong>Validated</strong> for <strong>ChIP-seq</strong> with multiple transcription factors and non-histone targets<br /></span></li>
<li><span style="font-weight: 400;"><strong>Most complete kit</strong> available (covers all steps, including the control antibodies and primers)<br /></span></li>
<li><span style="font-weight: 400;"><strong>Magnetic beads</strong> make ChIP <strong>easy</strong>, <strong>fast</strong> and more <strong>reproducible</strong></span></li>
<li><span style="font-weight: 400;">Combination with Diagenode ChIP-seq antibodies provides <strong>high yields</strong> with excellent <strong>specificity</strong> and <strong>sensitivity</strong><br /></span></li>
<li><span style="font-weight: 400;">Purified DNA suitable for any downstream application</span></li>
<li><span style="font-weight: 400;">Easy-to-follow protocol</span></li>
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<p><span style="font-weight: 400;"></span></p>
<p>&nbsp;</p>
<h3>ChIP-seq on cells</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-ctcf-diagenode.jpg" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1.</strong> (A) Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the GAPDH positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-b-total-diagendoe-peaks.png" alt="CTCF Diagenode" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 1B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>
<p>&nbsp;</p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-A.png" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-B.png" alt="ChIP-seq figure B" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-TF-chip-seq-C.png" alt="ChIP-seq figure C" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 2.</strong> Chromatin Immunoprecipitation has been performed using chromatin from HeLa cells, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade HDAC1 (A), LSD1 (B) and p53 antibody (C). The IP'd DNA was subsequently analysed on an Illumina<sup>&reg;</sup> Genome Analyzer. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in regions of chromosome 3 (A), chromosome 12 (B) and chromosome 6 (C) respectively.</p>
<p>&nbsp;</p>
<h3>ChIP-seq on tissue</h3>
<p><img src="https://www.diagenode.com/img/product/kits/ideal-figure-3a.jpg" alt="ChIP-seq figure A" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3A.</strong> Chromatin Immunoprecipitation has been performed using chromatin from mouse liver tissue, the iDeal ChIP-seq kit for Transcription Factors and the Diagenode ChIP-seq-grade CTCF antibody. The IP'd DNA was subsequently analysed on an Illumina&reg; HiSeq. Library preparation, cluster generation and sequencing were performed according to the manufacturer's instructions. This figure shows the peak distribution in a region surrounding the Vwf positive control gene.</p>
<p><img src="https://www.diagenode.com/img/product/kits/match-of-the-top40-peaks.png" alt="Match of the Top40 peaks" style="display: block; margin-left: auto; margin-right: auto;" /></p>
<p><strong>Figure 3B.</strong> The ChIP-seq dataset from this experiment has been compared with a reference dataset from the Broad Institute. We observed a perfect match between the top 40% of Diagenode peaks and the reference dataset. Based on the NIH Encode project criterion, ChIP-seq results are considered reproducible between an original and reproduced dataset if the top 40% of peaks have at least an 80% overlap ratio with the compared dataset.</p>',
	'label2' => 'Species, cell lines, tissues tested',
	'info2' => '<p>The iDeal ChIP-seq Kit for Transcription Factors is compatible with a broad variety of cell lines, tissues and species - some examples are shown below. Other species / cell lines / tissues can be used with this kit.</p>
<p><span style="text-decoration: underline;">Cell lines:</span></p>
<p>Human: A549, A673, BT-549, CD4 T, HCC1806, HeLa, HepG2, HFF, HK-GFP-MR, ILC,&nbsp;K562, KYSE-180, LapC4, M14, MCF7, MDA-MB-231, MDA-MB-436, RDES, SKNO1, VCaP, U2-OS, ZR-75-1&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;&nbsp;</p>
<p>Mouse: ESC, NPCs, BZ, GT1-7, acinar cells, HSPCs, Th2 cells, keratinocytes</p>
<p>Cattle: pbMEC, <span>MAC-T</span></p>
<p><span>Other cell lines / species: compatible, not tested</span></p>
<p><span style="text-decoration: underline;">Tissues:</span></p>
<p>Mouse: kidney, heart, brain, iris, liver, limbs from E10.5 embryos</p>
<p><span>Horse: l</span>iver, brain, heart, lung, skeletal muscle, lamina, ovary</p>
<p>Other tissues: compatible, not tested</p>
<p><span style="text-decoration: underline;">ChIP on yeast</span></p>
<p>The iDeal ChIP-seq kit for TF is compatible with yeast samples. Check out our <strong><a href="https://www.diagenode.com/files/products/kits/Application_Note-ChIP_on_Yeast.pdf">Application Note</a></strong>&nbsp;presenting an optimized detailed protocol for ChIP on yeast.</p>
<p></p>
<p>Did you use the iDeal ChIP-seq for Transcription Factors Kit on other cell line / tissue / species? <a href="mailto:agnieszka.zelisko@diagenode.com?subject=Species, cell lines, tissues tested with the iDeal ChIP-seq Kit for TF&amp;body=Dear Customer,%0D%0A%0D%0APlease, leave below your feedback about the iDeal ChIP-seq for Transcription Factors (cell / tissue type, species, other information...).%0D%0A%0D%0AThank you for sharing with us your experience !%0D%0A%0D%0ABest regards,%0D%0A%0D%0AAgnieszka Zelisko-Schmidt, PhD">Let us know!</a></p>',
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	'info3' => '<p><span style="font-weight: 400;">The</span> <a href="https://www.diagenode.com/en/p/chromatin-shearing-optimization-kit-low-sds-for-tfs-25-rxns"><span style="font-weight: 400;">Chromatin EasyShear Kit &ndash; Low SDS </span></a><span style="font-weight: 400;">is the kit compatible with the iDeal ChIP-seq kit for TF, recommended for the optimization of chromatin shearing, a critical step for ChIP.</span></p>
<p><a href="https://www.diagenode.com/en/p/chip-cross-link-gold-600-ul"><span style="font-weight: 400;">ChIP Cross-link Gold</span></a> <span style="font-weight: 400;">should be used in combination with formaldehyde when working with higher order and/or dynamic interactions, for efficient protein-protein fixation.</span></p>
<p><span style="font-weight: 400;">For library preparation of immunoprecipitated samples we recommend to use the </span><b>&nbsp;</b><a href="https://www.diagenode.com/en/categories/library-preparation-for-ChIP-seq"><span style="font-weight: 400;">MicroPlex Library Preparation Kit</span></a><span style="font-weight: 400;"> - validated for library preparation from picogram inputs.</span></p>
<p><a href="https://www.diagenode.com/en/categories/chip-seq-grade-antibodies"><span style="font-weight: 400;">ChIP-seq grade antibodies</span></a><span style="font-weight: 400;"> provide high yields with excellent specificity and sensitivity.</span></p>
<p><span style="font-weight: 400;">Check the list of available </span><a href="https://www.diagenode.com/en/categories/primer-pairs"><span style="font-weight: 400;">Primer pairs</span></a><span style="font-weight: 400;"> designed for high specificity to specific genomic regions.</span></p>
<p><span style="font-weight: 400;">Plus, for our <a href="https://www.diagenode.com/en/categories/ip-star">IP-Star Automation</a> users for automated ChIP, check out our <a href="https://www.diagenode.com/en/p/auto-ideal-chip-seq-kit-for-transcription-factors-x24-24-rxns">automated version</a> of this kit.</span></p>',
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	'name' => 'EPOP Functionally Links Elongin and Polycomb in Pluripotent Stem Cells',
	'authors' => 'Beringer M. et al.',
	'description' => '<p>The cellular plasticity of pluripotent stem cells is thought to be sustained by genomic regions that display both active and repressive chromatin properties. These regions exhibit low levels of gene expression, yet the mechanisms controlling these levels remain unknown. Here, we describe Elongin BC as a binding factor at the promoters of bivalent sites. Biochemical and genome-wide analyses show that Elongin BC is associated with Polycomb Repressive Complex 2 (PRC2) in pluripotent stem cells. Elongin BC is recruited to chromatin by the PRC2-associated&nbsp;factor EPOP (Elongin BC and Polycomb Repressive Complex 2 Associated Protein, also termed C17orf96, esPRC2p48, E130012A19Rik), a protein expressed in the inner cell mass of the mouse blastocyst. Both EPOP and Elongin BC are required to maintain low levels of expression at PRC2 genomic targets. Our results indicate that keeping the balance between activating and repressive cues is a more general feature of chromatin in pluripotent stem cells than previously appreciated.</p>',
	'date' => '2016-11-17',
	'pmid' => 'https://www.ncbi.nlm.nih.gov/pubmed/27863225',
	'doi' => '',
	'modified' => '2017-01-03 16:02:21',
	'created' => '2017-01-03 16:02:21',
	'ProductsPublication' => array(
		'id' => '1805',
		'product_id' => '1866',
		'publication_id' => '3105'
	)
)
$externalLink = ' <a href="https://www.ncbi.nlm.nih.gov/pubmed/27863225" target="_blank"><i class="fa fa-external-link"></i></a>'
include - APP/View/Products/view.ctp, line 755
View::_evaluate() - CORE/Cake/View/View.php, line 971
View::_render() - CORE/Cake/View/View.php, line 933
View::render() - CORE/Cake/View/View.php, line 473
Controller::render() - CORE/Cake/Controller/Controller.php, line 963
ProductsController::slug() - APP/Controller/ProductsController.php, line 1052
ReflectionMethod::invokeArgs() - [internal], line ??
Controller::invokeAction() - CORE/Cake/Controller/Controller.php, line 491
Dispatcher::_invoke() - CORE/Cake/Routing/Dispatcher.php, line 193
Dispatcher::dispatch() - CORE/Cake/Routing/Dispatcher.php, line 167
[main] - APP/webroot/index.php, line 118

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