PERK in the life and death of the pancreatic beta-cell.
To ensure cellular survival to ER (endoplasmic reticulum) stress, PERK [PKR (double-stranded-RNA-dependent protein kinase)-like ER kinase], an ER transmembrane kinase, is activated as part of the unfolded protein response. PERK is highly expressed in pancreatic beta-cells and is essential in the beta-cell's development, differentiation and function. However, chronic activation of PERK can induce cell death, and its activation has been implicated in both Type 1 and Type 2 diabetes. This short review aims to provide an insight into our current understanding of the role of PERK in the life and death of the beta-cell.
Herbert
T P
TP
Department of Cell Physiology and Pharmacology, The Henry Wellcome Building, University of Leicester, University Road, Leicester LE1 9HN, U.K. tph4@le.ac.uk
D000818:Animals; D002454:Cell Differentiation; D049109:Cell Proliferation; D005947:Glucose / Q000378:metabolism; D007515:Islets of Langerhans / Q000166:cytology*; D051379:Mice; D018345:Mice, Knockout
D005947:Glucose