title: Endoplasmic reticulum stress reduces COPII vesicle formation and modifies Sec23a cycling at ERESs.
abstract: Exit from the Endoplasmic Reticulum (ER) of newly synthesized proteins is mediated by COPII vesicles that bud from the ER at the ER Exit Sites (ERESs). Disruption of ER homeostasis causes accumulation of unfolded and misfolded proteins in the ER. This condition is referred to as ER stress. Previously, we demonstrated that ER stress rapidly impairs the formation of COPII vesicles. Here, we show that membrane association of COPII components, and in particular of Sec23a, is impaired by ER stress-inducing agents suggesting the existence of a dynamic interplay between protein folding and COPII assembly at the ER.
authors.affiliation: Dipartimento di Farmacia, Università degli Studi di Salerno, 84084 Fisciano, Salerno, Italy.
authors.forename: Giuseppina
authors.initials: G
authors.lastname: Amodio
authors.forename: Rossella
authors.initials: R
authors.lastname: Venditti
authors.forename: Maria Antonietta
authors.initials: MA
authors.lastname: De Matteis
authors.forename: Ornella
authors.initials: O
authors.lastname: Moltedo
authors.forename: Piero
authors.initials: P
authors.lastname: Pignataro
authors.forename: Paolo
authors.initials: P
authors.lastname: Remondelli
mesh_terms: D022181:COP-Coated Vesicles; D002460:Cell Line; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D059865:Endoplasmic Reticulum Stress; D006801:Humans; D011485:Protein Binding; D033921:Vesicular Transport Proteins / Q000378:metabolism*
chemical_list: C512739:SEC23A protein, human; D033921:Vesicular Transport Proteins
keywords: COPII; ER stress; ERES; Sec23