{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gong Y"],"funding":["China Scholarship Council","NIDDK NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases"],"pagination":["235"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9842633"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Glucagon has emerged as a key regulator of extracellular amino acid (AA) homeostasis. Insufficient glucagon signaling results in hyperaminoacidemia, which drives adaptive proliferation of glucagon-producing α cells. Aside from mammalian target of rapamycin complex 1 (mTORC1), the role of other AA sensors in α cell proliferation has not been described. Here, using both genders of mouse islets and glucagon receptor (gcgr)-deficient zebrafish (Danio rerio), we show α cell proliferation requires activation of the extracellular signal-regulated protein kinase (ERK1/2) by the AA-sensitive calcium sensing receptor (CaSR). Inactivation of CaSR dampened α cell proliferation, which was rescued by re-expression of CaSR or activation of Gq, but not Gi, signaling in α cells. CaSR was also unexpectedly "],"journal":["Nature communications"],"pubmed_title":["Hyperaminoacidemia induces pancreatic α cell proliferation via synergism between the mTORC1 and CaSR-Gq signaling pathways."],"pmcid":["PMC9842633"],"funding_grant_id":["T32 DK 7563-32","R01 DK117147","DK117969","K01 DK117969","T32 DK007563","202106260221","DK117147","(#201904910575"],"pubmed_authors":["Tang Z","Zhang D","Sellick K","Yang L","Shou M","Yang B","Siv WA","Coate KC","Powers AC","Gong Y","Chang W","Danielle Dean E","Covington BA","Zhang Y","Chen W","Patel RS","Yin L"],"additional_accession":[]},"is_claimable":false,"name":"Hyperaminoacidemia induces pancreatic α cell proliferation via synergism between the mTORC1 and CaSR-Gq signaling pathways.","description":"Glucagon has emerged as a key regulator of extracellular amino acid (AA) homeostasis. Insufficient glucagon signaling results in hyperaminoacidemia, which drives adaptive proliferation of glucagon-producing α cells. Aside from mammalian target of rapamycin complex 1 (mTORC1), the role of other AA sensors in α cell proliferation has not been described. Here, using both genders of mouse islets and glucagon receptor (gcgr)-deficient zebrafish (Danio rerio), we show α cell proliferation requires activation of the extracellular signal-regulated protein kinase (ERK1/2) by the AA-sensitive calcium sensing receptor (CaSR). Inactivation of CaSR dampened α cell proliferation, which was rescued by re-expression of CaSR or activation of Gq, but not Gi, signaling in α cells. CaSR was also unexpectedly ","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-05T12:56:46.51Z","creation":"2025-02-19T04:00:14.76Z"},"accession":"S-EPMC9842633","cross_references":{"pubmed":["36646689"],"doi":["10.1038/s41467-022-35705-4"]}}