The PERK phosphorylates the alpha subunit of eukaryotic translation-initiation factor 2 (EIF2), leading to its inactivation, and thus to a rapid reduction of translational initiation and repression of global protein synthesis. It is a type I membrane protein located in the endoplasmic reticulum (ER), where it is induced by ER stress caused by malfolded proteins. Research studies have demonstrated that PERK deficient mice have defects in pancreatic β cells several weeks after birth, suggesting a role for PERK mediated translational control in protecting secretory cells from ER stress.
