Histone deacetylase 4 represses dystrophin-glycoprotein (DGC) complex expression

ABSTRACT: Dysfunction of the dystrophin-glycoprotein complex (DGC) is a frequent cause of hereditary forms of muscular dystrophy. Although DGC function in maintaining skeletal muscle integrity has been well characterized, little is known about how the DGC complex is coordinately regulated at the transcriptional level. To test this hypothesis, we engineered HDAC4 stably overexpressing and control myotubes in an in vitro model of muscle differentiation. Here we present evidence that HDAC4, a neural activity-responsive histone deacetylase, is a critical transcriptional regulator of the DGC complex. We show that HDAC4 can repress multiple components of the DGC complex, including dystrophin and sarcoglycan family members in both cultured myotubes. To confirm this finding, the protein levels of core DG

ORGANISM(S): Mus musculus

SUBMITTER: Zachary Hartman 

PROVIDER: E-GEOD-10678 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress