{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["284(28)"],"submitter":["Gordon JW"],"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"],"journal":["The Journal of biological chemistry"],"pagination":["19027-42"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC2707197"],"repository":["biostudies-literature"],"pubmed_title":["Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells."],"pmcid":["PMC2707197"],"pubmed_authors":["Gordon JW","Bendeck MP","Pagiatakis C","Courtman D","Dan Q","Salma J","McDermott JC","Zhao J","Du M","Andreucci JJ","Hou G","Perry RL"],"additional_accession":[]},"is_claimable":false,"name":"Protein kinase A-regulated assembly of a MEF2{middle dot}HDAC4 repressor complex controls c-Jun expression in vascular smooth muscle cells.","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","dates":{"release":"2009-01-01T00:00:00Z","publication":"2009 Jul","modification":"2025-04-18T22:31:38.094Z","creation":"2019-03-27T00:23:22Z"},"accession":"S-EPMC2707197","cross_references":{"pubmed":["19389706"],"doi":["10.1074/jbc.M109.000539","10.1074/jbc.m109.000539"]}}