{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tanaka Y"],"funding":["MEXT | Japan Society for the Promotion of Science","JEOL, Ltd.","MEXT | Japan Society for the Promotion of Science (JSPS)","Uehara Memorial Foundation","Japan IDDM network","Ono Medical Research Foundation","Uehara Memorial Foundation (UMF)"],"pagination":["4777-4802"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11549326"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["25(11)"],"pubmed_abstract":["Glucose-stimulated insulin secretion (GSIS) from pancreatic beta cells is a principal mechanism for systemic glucose homeostasis, of which regulatory mechanisms are still unclear. Here we show that kinesin molecular motor KIF5B is essential for GSIS through maintaining the voltage-gated calcium channel Ca<sub>V</sub>1.2 levels, by facilitating an Hsp70-to-Hsp90 chaperone exchange to pass through the quality control in the endoplasmic reticulum (ER). Phenotypic analyses of KIF5B conditional knockout (cKO) mouse beta cells revealed significant abolishment of glucose-stimulated calcium transients, which altered the behaviors of insulin granules via abnormally stabilized cortical F-actin. KIF5B and Hsp90 colocalize to microdroplets on ER sheets, where Ca<sub>V</sub>1.2 but not K<sub>ir</sub>6."],"journal":["EMBO reports"],"pubmed_title":["Kinesin-1 mediates proper ER folding of the Ca<sub>V</sub>1.2 channel and maintains mouse glucose homeostasis."],"pmcid":["PMC11549326"],"funding_grant_id":["JP20K06634","JP23000013 and JP16H06372","N.A."],"pubmed_authors":["Yang W","Tanaka Y","Ueno H","Farkhondeh A","Hirokawa N","Noda M"],"additional_accession":[]},"is_claimable":false,"name":"Kinesin-1 mediates proper ER folding of the Ca<sub>V</sub>1.2 channel and maintains mouse glucose homeostasis.","description":"Glucose-stimulated insulin secretion (GSIS) from pancreatic beta cells is a principal mechanism for systemic glucose homeostasis, of which regulatory mechanisms are still unclear. Here we show that kinesin molecular motor KIF5B is essential for GSIS through maintaining the voltage-gated calcium channel Ca<sub>V</sub>1.2 levels, by facilitating an Hsp70-to-Hsp90 chaperone exchange to pass through the quality control in the endoplasmic reticulum (ER). Phenotypic analyses of KIF5B conditional knockout (cKO) mouse beta cells revealed significant abolishment of glucose-stimulated calcium transients, which altered the behaviors of insulin granules via abnormally stabilized cortical F-actin. KIF5B and Hsp90 colocalize to microdroplets on ER sheets, where Ca<sub>V</sub>1.2 but not K<sub>ir</sub>6.","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-06-01T17:34:08.599Z","creation":"2025-04-06T18:25:24.652Z"},"accession":"S-EPMC11549326","cross_references":{"pubmed":["39322740"],"doi":["10.1038/s44319-024-00246-y"]}}