{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Pan J"],"funding":["Fundamental Research Funds for the Central Universities","Natural Science Foundation of Shandong Province","National Science Foundation of China","Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences","Taishan Scholarship"],"pagination":["0823"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12352791"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8"],"pubmed_abstract":["Alcoholic cardiomyopathy (ACM) is a type of dilated cardiomyopathy unrelated to ischemia, which develops as a consequence of chronic alcohol consumption. While ethanol-induced irreversible cardiomyocyte death is implicated in ACM development and progression, the precise molecular mechanisms involved are still obscure. In the current study, we demonstrate that ethanol exposure promotes receptor-interacting serine/threonine-protein kinase 1 (RIPK1) autophosphorylation and enhances pRIPK1-associated apoptosis and necroptosis in ACM models both in vivo and in vitro. Through co-immunoprecipitation (Co-IP) combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, we identified ubiquitin-specific protease 53 (USP53) as a pivotal deubiquitinase involved in modulating RIPK1 "],"journal":["Research (Washington, D.C.)"],"pubmed_title":["USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377."],"pmcid":["PMC12352791"],"funding_grant_id":["2022HWYQ-053","tsqn202306035","ZR2022QH262","2023-PT320-06","2023HWYQ-048","ZR2024MH154","ZR2022QH005","2023QNTD003","82271757","82400525","82200660"],"pubmed_authors":["Liu X","Li X","Yuan C","Pan J","Dai S","Wang S","Zhang M","Liu D","Zhao Y","Liu F","Wang L"],"additional_accession":[]},"is_claimable":false,"name":"USP53 Drives Ethanol-Induced Myocardial Injury by Promoting K63 Deubiquitination-Dependent RIPK1 Activation at K377.","description":"Alcoholic cardiomyopathy (ACM) is a type of dilated cardiomyopathy unrelated to ischemia, which develops as a consequence of chronic alcohol consumption. While ethanol-induced irreversible cardiomyocyte death is implicated in ACM development and progression, the precise molecular mechanisms involved are still obscure. In the current study, we demonstrate that ethanol exposure promotes receptor-interacting serine/threonine-protein kinase 1 (RIPK1) autophosphorylation and enhances pRIPK1-associated apoptosis and necroptosis in ACM models both in vivo and in vitro. Through co-immunoprecipitation (Co-IP) combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis, we identified ubiquitin-specific protease 53 (USP53) as a pivotal deubiquitinase involved in modulating RIPK1 ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025","modification":"2026-05-29T16:32:24.408Z","creation":"2026-04-08T05:25:39.24Z"},"accession":"S-EPMC12352791","cross_references":{"pubmed":["40822127"],"doi":["10.34133/research.0823"]}}