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Publication : Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class II histone deacetylases.

First Author  Lu J Year  2000
Journal  Mol Cell Volume  6
Issue  2 Pages  233-44
PubMed ID  10983972 Mgi Jnum  J:152667
Mgi Id  MGI:4359371 Doi  10.1016/s1097-2765(00)00025-3
Citation  Lu J, et al. (2000) Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class II histone deacetylases. Mol Cell 6(2):233-44
abstractText  Skeletal muscle differentiation is controlled by associations between myogenic basic-helix-loop-helix and MEF2 transcription factors. We show that chromatin associated with muscle genes regulated by these transcription factors becomes acetylated during myogenesis and that class II histone deacetylases (HDACs), which interact with MEF2, specifically suppress myoblast differentiation. These HDACs do not interact directly with MyoD, yet they suppress its myogenic activity through association with MEF2. Elevating the level of MyoD can override the repression imposed by HDACs on muscle genes. HDAC-mediated repression of myogenesis also can be overcome by CaM kinase and insulin-like growth factor (IGF) signaling. These findings reveal central roles for HDACs in chromatin remodeling during myogenesis and as intranuclear targets for signaling pathways controlled by IGF and CaM kinase.
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