<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>284(28)</volume><submitter>Gordon JW</submitter><pubmed_abstract>Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression. Congruently, suppression of HDAC4 by RNA interference re</pubmed_abstract><journal>The Journal of biological chemistry</journal><pagination>19027-42</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2707197</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.</pubmed_title><pmcid>PMC2707197</pmcid><pubmed_authors>Gordon JW</pubmed_authors><pubmed_authors>Bendeck MP</pubmed_authors><pubmed_authors>Pagiatakis C</pubmed_authors><pubmed_authors>Courtman D</pubmed_authors><pubmed_authors>Dan Q</pubmed_authors><pubmed_authors>Salma J</pubmed_authors><pubmed_authors>McDermott JC</pubmed_authors><pubmed_authors>Zhao J</pubmed_authors><pubmed_authors>Du M</pubmed_authors><pubmed_authors>Andreucci JJ</pubmed_authors><pubmed_authors>Hou G</pubmed_authors><pubmed_authors>Perry RL</pubmed_authors></additional><is_claimable>false</is_claimable><name>Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.</name><description>Vascular smooth muscle cells (VSMCs) maintain the ability to modulate their phenotype in response to changing environmental stimuli. This phenotype modulation plays a critical role in the development of most vascular disease states. In these studies, stimulation of cultured vascular smooth muscle cells with platelet-derived growth factor resulted in marked induction of c-jun expression, which was attenuated by protein kinase Cdelta and calcium/calmodulin-dependent protein kinase inhibition. Given that these signaling pathways have been shown to relieve the repressive effects of class II histone deacetylases (HDACs) on myocyte enhancer factor (MEF) 2 proteins, we ectopically expressed HDAC4 and observed repression of c-jun expression. Congruently, suppression of HDAC4 by RNA interference re</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Jul</publication><modification>2025-04-18T22:31:38.094Z</modification><creation>2019-03-27T00:23:22Z</creation></dates><accession>S-EPMC2707197</accession><cross_references><pubmed>19389706</pubmed><doi>10.1074/jbc.M109.000539</doi><doi>10.1074/jbc.m109.000539</doi></cross_references></HashMap>