Role of the Interaction Between NCK1 and PERK in Pancreatic Beta-cell Function and Survival

Abstract

Preventing pancreatic β-cell failure and death, features of diabetes pathogenesis, could help treat diabetes. PERK (Protein Kinase R–Like Endoplasmic Reticulum Kinase), a player in the unfolded protein response, is essential for β-cell function and survival. PERK activity is modulated by binding of the adaptor protein NCK1 (Non-Catalytic region of tyrosine Kinase). Silencing of Nck1 in β cells in vitro enhances basal PERK activity and prevents its pathological hyperactivation under diabetogenic stresses, improving β-cell function and survival.