PERK leads a hub dictating pancreatic cell homoeostasis

In humans, the pathogenesis of diabetes is characterised by two major pancreatic cell defects: a reduction in cell mass and the failure of cells to produce enough insulin. Over the past two decades, multiple studies involving cell cultures, animal models and human subjects have established the importance of the protein kinase RNA-like endoplasmic reticulum kinase (PERK) in the adaptive functional capacity of pancreatic cells during embryonic development and into adulthood. In this review, we will highlight major findings identifying PERK as a crucial player in cell physiology and in diabetes.