In this study, we report that endogenous HDAC4 and HDAC5 in VSM are activated in a Ca 2+ - and CaMKIIδ2-dependent manner. We further show that AngII-and PDGF-dependent phosphorylation of HDAC4 and HDAC5 is reduced when CaMKIIδ2 expression is suppressed or CaMKIIδ2 activity is attenuated.

In osteocytes, HDAC5 binds and inhibits the function of MEF2C, a crucial transcription factor for SOST expression. Using chromatin immunoprecipitation, we have mapped endogenous MEF2C binding in the SOST gene to a distal intergenic enhancer 45 …

Consistently, cAMP-induced repression of agonist-driven cellular hypertrophy was blunted in cardiomyocytes deficient for both HDAC5 and HDAC4. In conclusion, cAMP inhibits MEF2 through both nuclear accumulation of hypo-phosphorylated HDAC5 and through a distinct HDAC4-dependent mechanism.

Nov 1, 2015 · To clarify the apparent paradox of the MEF2-dependent transcriptional stimulation coupled to the upregulation of HDAC5 and HDAC9 mRNA levels, we performed an absolute quantification of class-IIa HDAC expression (Fig. 2C).

Our findings provide an unexpected new link between inflammation and cardiac remodeling by de‐repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.

Nov 2, 2000 · Execution of the muscle differentiation program requires release of MEF2 from repression by HDACs, which are expressed constitutively in myoblasts and myotubes 5. Here we show that HDAC5...

HDAC4 is believed to repress MEF2 transcriptional activity by binding to MEF2 and catalyzing local histone deacetylation. Here we report that HDAC4 also controls MEF2 by a novel SUMO E3 ligase activity. We show that HDAC4 interacts with the SUMO E2 conjugating enzyme Ubc9 and is itself sumoylated.

Jul 23, 2020 · HDAC5 has been identified as a repressor of MEF2C transcriptional activity through the binding of HDAC5 on its MEF2-binding domain (Figure 3 B). We next quantified the mRNA expression levels of Hdac5 in both SC and EE visual cortices.

In osteocytes, HDAC5 binds and inhibits the function of MEF2C, a crucial transcription factor for SOST expression. Using chromatin immunoprecipitation, we have mapped endogenous MEF2C binding in the SOST gene to a distal intergenic enhancer 45 …

Mar 25, 2017 · MEF2 is a well‐characterized binding partner of HDAC5, and disruption of their interaction following phosphorylation‐dependent nuclear export of HDAC5 permits MEF2‐dependent gene transcription that promotes maladaptive cardiomyocyte hypertrophy. 13, 15, 27 Relative to the heterologous expression of GFP alone, that of WT GFP‐HDAC5 ...