open access

https://hdl.handle.net/2115/1426

PI3K-Akt inactivation induced CHOP expression in endoplasmic reticulum-stressed cells

英語

CHOP

2006-02

Elsevier Inc.

Biochemical and Biophysical Research Communications

340(1)

286-290

http://www.sciencedirect.com/science/journal/0006291X

Stress signals that impair the function of the endoplasmic reticulum (ER) can lead to an accumulation of unfolded proteins in the ER causing cell death. Recent studies have indicated that ER stress contributes to several diseases such as neurodegenerative disorders or diabetes. In the present study, we found that Akt down-regulation is important for inducing CHOP expression, an ER stress-induced transcription factor. Treatment with tunicamycin or thapsigargin, ER stress inducers, caused dephosphorylation of Akt from 12 to 24 h and induced cell death. Interestingly, treatment with a PI3K inhibitor alone induced CHOP expression and caused cell death. However, a MEK1 inhibitor induced neither CHOP expression nor cell death. These results indicate that the inactivation of Akt by ER stress induces CHOP expression and causes cell death. Therefore, Akt plays an important role in ER stressed condition and may have important implications for understanding ER stress-related diseases.

学術雑誌論文

Accepted Manuscript

0006-291X