Roles of CHOP/GADD153 in endoplasmic reticulum stress

被引:2366
|
作者
Oyadomari, S [1 ]
Mori, M [1 ]
机构
[1] Kumamoto Univ, Grad Sch Med Sci, Dept Mol Genet, Kumamoto 8608556, Japan
来源
CELL DEATH AND DIFFERENTIATION | 2004年 / 11卷 / 04期
关键词
endoplasmic reticulum; transcription factor; apoptosis; pancreatic cells; diabetes; nitric oxide;
D O I
10.1038/sj.cdd.4401373
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:381 / 389
页数:9
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