Differences in endoplasmic reticulum stress signalling kinetics determine cell survival outcome through activation of MKP-1

2011 ◽  
Vol 23 (1) ◽  
pp. 35-45 ◽  
Author(s):  
Bin Li ◽  
Ping Yi ◽  
Bi Zhang ◽  
Chanjuan Xu ◽  
Qiuyao Liu ◽  
...  
Toxins ◽  
2018 ◽  
Vol 10 (6) ◽  
pp. 239 ◽  
Author(s):  
Barbara Canonico ◽  
Gianna Di Sario ◽  
Erica Cesarini ◽  
Raffaella Campana ◽  
Francesca Luchetti ◽  
...  

2008 ◽  
Vol 7 (3) ◽  
pp. 269-276 ◽  
Author(s):  
Suguru Yamaguchi ◽  
Hisamitsu Ishihara ◽  
Takahiro Yamada ◽  
Akira Tamura ◽  
Masahiro Usui ◽  
...  

2006 ◽  
Vol 282 (7) ◽  
pp. 4702-4710 ◽  
Author(s):  
Wen-Xing Ding ◽  
Hong-Min Ni ◽  
Wentao Gao ◽  
Yi-Feng Hou ◽  
Melissa A. Melan ◽  
...  

Autophagy is a cellular response to adverse environment and stress, but its significance in cell survival is not always clear. Here we show that autophagy could be induced in the mammalian cells by chemicals, such as A23187, tunicamycin, thapsigargin, and brefeldin A, that cause endoplasmic reticulum stress. Endoplasmic reticulum stress-induced autophagy is important for clearing polyubiquitinated protein aggregates and for reducing cellular vacuolization in HCT116 colon cancer cells and DU145 prostate cancer cells, thus mitigating endoplasmic reticulum stress and protecting against cell death. In contrast, autophagy induced by the same chemicals does not confer protection in a normal human colon cell line and in the non-transformed murine embryonic fibroblasts but rather contributes to cell death. Thus the impact of autophagy on cell survival during endoplasmic reticulum stress is likely contingent on the status of cells, which could be explored for tumor-specific therapy.


Nature ◽  
2008 ◽  
Vol 457 (7230) ◽  
pp. 736-740 ◽  
Author(s):  
Tomás Aragón ◽  
Eelco van Anken ◽  
David Pincus ◽  
Iana M. Serafimova ◽  
Alexei V. Korennykh ◽  
...  

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