Β-cell receptor tyrosine kinases in controlling insulin secretion and exocytotic machinery: C-kit and insulin receptor
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Insulin secretion from pancreatic β-cells is initiated through channel-mediated depolarization, cytoskeletal remodeling, and vesicle tethering at the cell membrane, all of which can be regulated through cell surface receptors. Receptor tyrosine kinases (RTKs) promote β-cell development and postnatal signaling to improve β-cell mass and function, yet their activation has also been shown to initiate exocytotic events in b-cells. This review examines the role of RTK signaling in insulin secretion, with a focus on RTKs c-Kit and insulin receptor (IR). Pathways that control insulin release and the potential interplay between c-Kit and IR signaling are discussed, along with clinical implications of RTK therapy on insulin secretion.