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A proposed model for the critical role of SAD-A in regulating insulin secretion through phosphorylation of GDIα at Ser174. An elevated level of cAMP, which was generated from activation of incretin hormone receptors and glucose metabolism, can trigger direct phosphorylation of key regulatory sites of GDIα at Ser174 by SAD-A, leading to full activation of GTPases, which stimulate cytoskeletal remodeling and GSIS. AC, adenylyl cyclase; GPCR, G protein–coupled receptors.
