Diagenode

Histone Deacetylase 6 is a FoxO transcription factor-dependent effector in skeletal muscle atrophy.


Ratti F, Ramond F, Moncollin V, Simonet T, Milan G, Mejat A, Thomas JL, Streichenberger N, Gilquin B, Matthias P, Khochbin S, Sandri M, Schaeffer L

Skeletal muscle atrophy is a severe condition of muscle mass loss. Muscle atrophy is caused by a downregulation of protein synthesis and by an increase of protein breakdown due to the ubiquitin-proteasome system and autophagy activation. Upregulation of specific genes, such as the muscle specific E3 ubiquitin ligase MAFbx, by FoxO transcription factors is essential to initiate muscle protein ubiquitination and degradation during atrophy. HDAC6 is a particular HDAC, which is functionally related to the ubiquitin proteasome system via its ubiquitin binding domain. We show that HDAC6 is upregulated during muscle atrophy. HDAC6 activation is dependent on the transcription factor FoxO3a, and the inactivation of HDAC6 in mice protects against muscle wasting. HDAC6 is able to interact with MAFbx, a key ubiquitin ligase involved in muscle atrophy. Our findings demonstrate the implication of HDAC6 in skeletal muscle wasting and identify HDAC6 as a new downstream target of FoxO3a in stress response. This work provides new insights in skeletal muscle atrophy development and opens interesting perspectives on HDAC6 as a valuable marker of muscle atrophy and a potential target for pharmacological treatments.

Tags
Bioruptor
Chromatin Shearing
ChIP-qPCR

Share this article

Published
December, 2014

Source

活动

  • AACR 2024
    San Diego, California, USA
    Apr 5-Apr 10, 2024
 查看所有活动

新闻

 查看所有新闻


The European Regional Development Fund and Wallonia are investing in your future.

Extension of industrial buildings and new laboratories.


       Site map   |   Contact us   |   Conditions of sales   |   Conditions of purchase   |   Privacy policy   |   Diagenode Diagnostics