Endoplasmic Reticulum stress reduces COPII vesicle formation and modifies Sec23a cycling at ERESs

2013/08/27 by Giuseppina Amodio, Rossella Venditti, Maria Antonietta De Matteis +3 · 14 citations
Biochemistry, Genetics and Molecular Biology · #Endoplasmic Reticulum Stress and Disease #Cellular transport and secretion #RNA regulation and disease

paper · doi:10.1016/j.febslet.2013.08.021

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.

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• Identification of Cysteine Ubiquitylation Sites on the Sec23A Protein of the COPII Complex Required for Vesicle Formation from the ER. [europepmc]
• The Endoplasmic Reticulum Unfolded Protein Response in Neurodegenerative Disorders and Its Potential Therapeutic Significance. [europepmc]
• Alteration of endosomal trafficking is associated with early-onset parkinsonism caused by SYNJ1 mutations. [europepmc]
• Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction. [europepmc]
• Effect of the unfolded protein response on ER protein export: a potential new mechanism to relieve ER stress. [europepmc]
• How to Avoid a No-Deal ER Exit. [europepmc]
• The Functional Role of SEC23 in Vesicle Transportation, Autophagy and Cancer. [europepmc]
• Alcohol-Induced Liver Injury: Down-regulation and Redistribution of Rab3D Results in Atypical Protein Trafficking. [europepmc]
• Autophagy-Associated IL-15 Production Is Involved in the Pathogenesis of Leprosy Type 1 Reaction. [europepmc]
• Sec23a inhibits the self-renewal of melanoma cancer stem cells via inactivation of ER-phagy. [europepmc]
• ER exit in physiology and disease. [europepmc]
• The impact of SEC23A on 5-FU chemotherapy sensitivity and its involvement in endoplasmic reticulum stress-induced apoptosis in colorectal cancer. [europepmc]
• Redox signaling-mediated S-glutathionylation of protein disulfide isomerase A1 initiates intrinsic apoptosis and contributes to accelerated aging. [europepmc]

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