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

FEBS Lett. 2013 Oct 1;587(19):3261-6. doi: 10.1016/j.febslet.2013.08.021. Epub 2013 Aug 27.


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.

Keywords: COPII; ER stress; ERES; Sec23.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • COP-Coated Vesicles*
  • Cell Line
  • Endoplasmic Reticulum / metabolism*
  • Endoplasmic Reticulum Stress*
  • Humans
  • Protein Binding
  • Vesicular Transport Proteins / metabolism*


  • SEC23A protein, human
  • Vesicular Transport Proteins