{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yang ZJ"],"funding":["NIA NIH HHS","NIAMS NIH HHS","NIGMS NIH HHS"],"pagination":["560-73"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4356341"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(4)"],"pubmed_abstract":["Acute muscle injury and physiological stress from chronic muscle diseases and aging lead to impairment of skeletal muscle function. This raises the question of whether p53, a cellular stress sensor, regulates muscle tissue repair under stress conditions. By investigating muscle differentiation in the presence of genotoxic stress, we discovered that p53 binds directly to the myogenin promoter and represses transcription of myogenin, a member of the MyoD family of transcription factors that plays a critical role in driving terminal muscle differentiation. This reduction of myogenin protein is observed in G1-arrested cells and leads to decreased expression of late but not early differentiation markers. In response to acute genotoxic stress, p53-mediated repression of myogenin reduces post-mitotic nuclear abnormalities in terminally differentiated cells. This study reveals a mechanistic link previously unknown between p53 and muscle differentiation, and suggests new avenues for managing p53-mediated stress responses in chronic muscle diseases or during muscle aging."],"journal":["Cell death and differentiation"],"pubmed_title":["p53 suppresses muscle differentiation at the myogenin step in response to genotoxic stress."],"pmcid":["PMC4356341"],"funding_grant_id":["P50 GM107615","R21 AG040360","5R21AG040360-02","R01 AR045113","R01 GM030179"],"pubmed_authors":["Yang ZJ","Ferreira JP","Meyer T","Attardi LD","Wang CL","Spencer SL","Broz DK","Noderer WL","Tapscott SJ","Overton KW"],"additional_accession":[]},"is_claimable":false,"name":"p53 suppresses muscle differentiation at the myogenin step in response to genotoxic stress.","description":"Acute muscle injury and physiological stress from chronic muscle diseases and aging lead to impairment of skeletal muscle function. This raises the question of whether p53, a cellular stress sensor, regulates muscle tissue repair under stress conditions. By investigating muscle differentiation in the presence of genotoxic stress, we discovered that p53 binds directly to the myogenin promoter and represses transcription of myogenin, a member of the MyoD family of transcription factors that plays a critical role in driving terminal muscle differentiation. This reduction of myogenin protein is observed in G1-arrested cells and leads to decreased expression of late but not early differentiation markers. In response to acute genotoxic stress, p53-mediated repression of myogenin reduces post-mitotic nuclear abnormalities in terminally differentiated cells. This study reveals a mechanistic link previously unknown between p53 and muscle differentiation, and suggests new avenues for managing p53-mediated stress responses in chronic muscle diseases or during muscle aging.","dates":{"release":"2015-01-01T00:00:00Z","publication":"2015 Apr","modification":"2026-04-14T19:25:52.893Z","creation":"2019-03-27T01:48:01Z"},"accession":"S-EPMC4356341","cross_references":{"pubmed":["25501595"],"doi":["10.1038/cdd.2014.189"]}}