PERK and filamin A in actin cytoskeleton remodeling at ER-plasma membrane contact sites
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Updated: Feb 20, 2026

In Vitro Polymerization of F-actin on Early Endosomes
Published on: August 28, 2017
Alexander R van Vliet1, Patrizia Agostinis1
1Department Cellular and Molecular Medicine, Laboratory of Cell Death and Therapy, KU Leuven, Leuven, Belgium.
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.
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