{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Qiao A"],"funding":["American Heart Association","American Diabetes Association"],"pagination":["11469"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9569775"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["23(19)"],"pubmed_abstract":["Hepatic glucose production (HGP) is an important component of glucose homeostasis, and deregulated HGP, particularly through gluconeogenesis, contributes to hyperglycemia and pathology of type-2 diabetes (T2D). It has been shown that the gluconeogenic gene expression is governed primarily by the transcription factor cAMP-response element (CRE)-binding protein (CREB) and its coactivator, CREB-regulated transcriptional coactivator 2 (CRTC2). Recently, we have discovered that Sam68, an adaptor protein and Src kinase substrate, potently promotes hepatic gluconeogenesis by promoting CRTC2 stability; however, the detailed mechanisms remain unclear. Here we show that in response to glucagon, Sam68 increases CREB/CRTC2 transactivity by interacting with CRTC2 in the CREB/CRTC2 complex and occupying"],"journal":["International journal of molecular sciences"],"pubmed_title":["Hepatic Sam68 Regulates Systemic Glucose Homeostasis and Insulin Sensitivity."],"pmcid":["PMC9569775"],"funding_grant_id":["19TPA34910227","1-15-BS-148","19CDA34630052"],"pubmed_authors":["Jiang Y","Qiao A","Yan B","Qin G","Han C","Ma W","Zhou J"],"additional_accession":[]},"is_claimable":false,"name":"Hepatic Sam68 Regulates Systemic Glucose Homeostasis and Insulin Sensitivity.","description":"Hepatic glucose production (HGP) is an important component of glucose homeostasis, and deregulated HGP, particularly through gluconeogenesis, contributes to hyperglycemia and pathology of type-2 diabetes (T2D). It has been shown that the gluconeogenic gene expression is governed primarily by the transcription factor cAMP-response element (CRE)-binding protein (CREB) and its coactivator, CREB-regulated transcriptional coactivator 2 (CRTC2). Recently, we have discovered that Sam68, an adaptor protein and Src kinase substrate, potently promotes hepatic gluconeogenesis by promoting CRTC2 stability; however, the detailed mechanisms remain unclear. Here we show that in response to glucagon, Sam68 increases CREB/CRTC2 transactivity by interacting with CRTC2 in the CREB/CRTC2 complex and occupying","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Sep","modification":"2026-06-20T03:23:19.145Z","creation":"2025-04-20T01:47:12.506Z"},"accession":"S-EPMC9569775","cross_references":{"pubmed":["36232770"],"doi":["10.3390/ijms231911469"]}}