PERK and filamin A in actin cytoskeleton remodeling at ER-plasma membrane contact sites

Abstract

The endoplasmic reticulum (ER) stress sensor protein kinase RNA-like endoplasmic reticulum kinase (PERK) plays a major role during the unfolded protein response (UPR), mainly through eIF2α phosphorylation. We uncovered that PERK, by interacting with Filamin A, elicits F-actin remodeling required for ER-plasma membrane contact site formation after ER-Ca2+ depletion, through a UPR-independent mechanism.

Keywords

• actin-cytoskeleton
• calcium flux
• contact sites
• endoplasmic reticulum stress
• filamin a
• perk
• stim1
• store operated calcium entry
• unfolded protein response