Roles of CHOP/GADD153 in endoplasmic reticulum stress

Cell Death Differ. 2004 Apr;11(4):381-9. doi: 10.1038/sj.cdd.4401373.


Endoplasmic reticulum (ER) is the site of synthesis and folding of secretory proteins. Perturbations of ER homeostasis affect protein folding and cause ER stress. ER can sense the stress and respond to it through translational attenuation, upregulation of the genes for ER chaperones and related proteins, and degradation of unfolded proteins by a quality-control system. However, when the ER function is severely impaired, the organelle elicits apoptotic signals. ER stress has been implicated in a variety of common diseases such as diabetes, ischemia and neurodegenerative disorders. One of the components of the ER stress-mediated apoptosis pathway is C/EBP homologous protein (CHOP), also known as growth arrest- and DNA damage-inducible gene 153 (GADD153). Here, we summarize the current understanding of the roles of CHOP/GADD153 in ER stress-mediated apoptosis and in diseases including diabetes, brain ischemia and neurodegenerative disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / physiology
  • CCAAT-Enhancer-Binding Proteins / chemistry
  • CCAAT-Enhancer-Binding Proteins / metabolism*
  • Cell Differentiation / physiology
  • Cell Division / physiology
  • Disease / etiology
  • Endoplasmic Reticulum / metabolism*
  • Humans
  • Mice
  • Stress, Physiological / metabolism*
  • Transcription Factor CHOP
  • Transcription Factors / chemistry
  • Transcription Factors / metabolism*


  • CCAAT-Enhancer-Binding Proteins
  • DDIT3 protein, human
  • Ddit3 protein, mouse
  • Transcription Factors
  • Transcription Factor CHOP