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. 2023 Feb 21;299(4):103045. doi: 10.1016/j.jbc.2023.103045

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© 2023 The Authors

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

GIV acutely promotes Nephrin-dependent glucose-stimulated insulin secretion via actin cytoskeleton reorganization in β cells. (1) Src kinase induced GIV-Y1767 phosphorylation in response to elevated glucose. (2) GIV-Y1767 phosphorylation recruited Src kinase to Nephrin for phosphorylating Nephrin. (3) Nephrin phosphorylation induced Nephrin endocytosis pathway. (4) Cytoplasm Nephrin from endocytosis and PI3K/Akt signaling regulated activities of actin-modulatory protein Rac1 and RhoA, to (5) permeabilize a peripheral F-actin barrier, and (6) promoted insulin granule exocytosis.