{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hamoud N"],"funding":["NIDDK NIH HHS"],"pagination":["4470"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC6203814"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(1)"],"pubmed_abstract":["Myoblast fusion is tightly regulated during development and regeneration of muscle fibers. BAI3 is a receptor that orchestrates myoblast fusion via Elmo/Dock1 signaling, but the mechanisms regulating its activity remain elusive. Here we report that mice lacking BAI3 display small muscle fibers and inefficient muscle regeneration after cardiotoxin-induced injury. We describe two proteins that repress or activate BAI3 in muscle progenitors. We find that the secreted C1q-like1-4 proteins repress fusion by specifically interacting with BAI3. Using a proteomic approach, we identify Stabilin-2 as a protein that interacts with BAI3 and stimulates its fusion promoting activity. We demonstrate that Stabilin-2 activates the GPCR activity of BAI3. The resulting activated heterotrimeric G-proteins con"],"journal":["Nature communications"],"pubmed_title":["Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion."],"pmcid":["PMC6203814"],"funding_grant_id":["R01 DK084171"],"pubmed_authors":["Cote JF","Bouvier M","Lahaie S","Kania A","Tran V","Kim IS","Yuzaki M","Thibault MP","Wong GW","Hamoud N","Aimi T","Kakegawa W","Pelletier A"],"additional_accession":[]},"is_claimable":false,"name":"Spatiotemporal regulation of the GPCR activity of BAI3 by C1qL4 and Stabilin-2 controls myoblast fusion.","description":"Myoblast fusion is tightly regulated during development and regeneration of muscle fibers. BAI3 is a receptor that orchestrates myoblast fusion via Elmo/Dock1 signaling, but the mechanisms regulating its activity remain elusive. Here we report that mice lacking BAI3 display small muscle fibers and inefficient muscle regeneration after cardiotoxin-induced injury. We describe two proteins that repress or activate BAI3 in muscle progenitors. We find that the secreted C1q-like1-4 proteins repress fusion by specifically interacting with BAI3. Using a proteomic approach, we identify Stabilin-2 as a protein that interacts with BAI3 and stimulates its fusion promoting activity. We demonstrate that Stabilin-2 activates the GPCR activity of BAI3. The resulting activated heterotrimeric G-proteins con","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Oct","modification":"2025-04-22T16:04:36.947Z","creation":"2019-03-27T00:04:34Z"},"accession":"S-EPMC6203814","cross_references":{"pubmed":["30367035"],"doi":["10.1038/s41467-018-06897-5"]}}