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2. Pancreas-specific SNAP23 depletion prevents pancreatitis by attenuating pathological basolateral exocytosis and formation of trypsin-activating autolysosomes

4. SNAP23 depletion enables more SNAP25/calcium channel excitosome formation to increase insulin exocytosis in type 2 diabetes

6. Kv2.1 clusters on β-cell plasma membrane act as reservoirs that replenish pools of newcomer insulin granule through their interaction with syntaxin-3

7. Pancreatitis-Induced Depletion of Syntaxin 2 Promotes Autophagy and Increases Basolateral Exocytosis

8. Depletion of the membrane-fusion regulator Munc18c attenuates caerulein hyperstimulation–induced pancreatitis

11. Munc18b Increases Insulin Granule Fusion, Restoring Deficient Insulin Secretion in Type-2 Diabetes Human and Goto-Kakizaki Rat Islets with Improvement in Glucose Homeostasis

12. Syntaxin 2 Acts as Inhibitory SNARE for Insulin Granule Exocytosis

18. Munc18b Is a Major Mediator of Insulin Exocytosis in Rat Pancreatic β-Cells

20. RalA GTPase Tethers Insulin Granules to L- and R-Type Calcium Channels Through Binding α2δ-1 Subunit

22. Dual Role of VAMP8 in Regulating Insulin Exocytosis and Islet β Cell Growth

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