{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tian X"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["823"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9512921"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(9)"],"pubmed_abstract":["Liver ischemia/reperfusion (I/R) injury is a major clinical concern of liver transplantation, which accounts for organ rejection and liver dysfunction. The adaptor protein p66Shc acts as a crucial redox enzyme and is implicated in liver I/R. Elevated p66Shc expression is associated with hepatocellular apoptosis in liver I/R, but the molecular mechanisms of p66Shc responsible for its aberrant expression and function remain unknown. In the present study, hepatocyte-specific p66Shc-knockdown mice exhibited clear inhibition in hepatocellular apoptosis and oxidative stress under liver I/R, while hepatocyte-specific p66Shc overexpression mice displayed the deteriorative impairment. Mechanistically, p66Shc-triggered mitochondrial fission and apoptosis in liver I/R by mediating ROS-driven Drp1 act"],"journal":["Cell death & disease"],"pubmed_title":["USP15 regulates p66Shc stability associated with Drp1 activation in liver ischemia/reperfusion."],"pmcid":["PMC9512921"],"funding_grant_id":["81721091"],"pubmed_authors":["Zhou L","Yang Z","Tian X","Zheng S","Zhao Y","Lu Q"],"additional_accession":[]},"is_claimable":false,"name":"USP15 regulates p66Shc stability associated with Drp1 activation in liver ischemia/reperfusion.","description":"Liver ischemia/reperfusion (I/R) injury is a major clinical concern of liver transplantation, which accounts for organ rejection and liver dysfunction. The adaptor protein p66Shc acts as a crucial redox enzyme and is implicated in liver I/R. Elevated p66Shc expression is associated with hepatocellular apoptosis in liver I/R, but the molecular mechanisms of p66Shc responsible for its aberrant expression and function remain unknown. In the present study, hepatocyte-specific p66Shc-knockdown mice exhibited clear inhibition in hepatocellular apoptosis and oxidative stress under liver I/R, while hepatocyte-specific p66Shc overexpression mice displayed the deteriorative impairment. Mechanistically, p66Shc-triggered mitochondrial fission and apoptosis in liver I/R by mediating ROS-driven Drp1 act","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2025-04-22T06:24:48.316Z","creation":"2025-04-05T21:41:47.722Z"},"accession":"S-EPMC9512921","cross_references":{"pubmed":["36163170"],"doi":["10.1038/s41419-022-05277-8"]}}