{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aye CC"],"funding":["European Commission, Framework 7"],"pagination":["3399"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9964740"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["24(4)"],"pubmed_abstract":["CBL is rapidly phosphorylated upon insulin receptor activation. Mice whole body CBL depletion improved insulin sensitivity and glucose clearance; however, the precise mechanisms remain unknown. We depleted either CBL or its associated protein SORBS1/CAP independently in myocytes and assessed mitochondrial function and metabolism compared to control cells. CBL- and CAP-depleted cells showed increased mitochondrial mass with greater proton leak. Mitochondrial respiratory complex I activity and assembly into respirasomes were reduced. Proteome profiling revealed alterations in proteins involved in glycolysis and fatty acid degradation. Our findings demonstrate CBL/CAP pathway couples insulin signaling to efficient mitochondrial respiratory function and metabolism in muscle."],"journal":["International journal of molecular sciences"],"pubmed_title":["CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells."],"pmcid":["PMC9964740"],"funding_grant_id":["HEALTH-F4-2008-223450"],"pubmed_authors":["Vidal-Puig A","Perez-Perez R","Diaz-Ramos A","Rodriguez-Cuenca S","Yang C","Ugalde C","Doherty MK","Aye CC","Li X","Mora S","Phelan MM","Hammond DE","Zorzano A","Oresic M","Whitfield PD","Peddinti G"],"additional_accession":[]},"is_claimable":false,"name":"CBL/CAP Is Essential for Mitochondria Respiration Complex I Assembly and Bioenergetics Efficiency in Muscle Cells.","description":"CBL is rapidly phosphorylated upon insulin receptor activation. Mice whole body CBL depletion improved insulin sensitivity and glucose clearance; however, the precise mechanisms remain unknown. We depleted either CBL or its associated protein SORBS1/CAP independently in myocytes and assessed mitochondrial function and metabolism compared to control cells. CBL- and CAP-depleted cells showed increased mitochondrial mass with greater proton leak. Mitochondrial respiratory complex I activity and assembly into respirasomes were reduced. Proteome profiling revealed alterations in proteins involved in glycolysis and fatty acid degradation. Our findings demonstrate CBL/CAP pathway couples insulin signaling to efficient mitochondrial respiratory function and metabolism in muscle.","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Feb","modification":"2025-04-26T00:05:30.055Z","creation":"2025-04-06T09:34:53.96Z"},"accession":"S-EPMC9964740","cross_references":{"pubmed":["36834818"],"doi":["10.3390/ijms24043399"]}}