Figure 1.

Insulin secretion mechanism and the role of CAV1. At high glucose conditions, the increased ATP/ADP ratio results in the closure of the ATP-sensitive K⁺ channel K_v2.1, which in turn prompts the opening of the voltage-dependent Ca²⁺ channel Ca_v1.2. The increased cytoplasmic Ca²⁺ triggers the activation of exocytotic machinery. The process is initiated by the dissociation of the CAV1-cdc42-GDP complex through CAV1^Tyr14 phosphorylation. The released inactive cdc42-GDP binds to βPIX resulting in an active cdc42-GTP, which interacts with VAMP2-bound insulin secretory granules. These vesicles are then targeted to fusion with the plasma membrane through the interaction between cdc42, VAMP2, F-actin, Syntaxin 1A, and SNAP-25 modulations. Abbreviations: β cell—pancreatic β cell line; GLUT—glucose transporter; TCA cycle—tricarboxylic acid cycle or Krebs cycle; cdc42—cell division cycle 42; βPIX—guanine nucleotide exchange factor 7; VAMP2—vesicle-associated membrane protein 2; F-actin—filamentous actin; SNAP-25—synaptosomal-associated protein 25.