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PI3K-Akt inactivation induced CHOP expression in endoplasmic reticulum-stressed cells
| Title: | PI3K-Akt inactivation induced CHOP expression in endoplasmic reticulum-stressed cells |
| Authors: | Hyoda, Kanae Browse this author | | Hosoi, Toru Browse this author | | Horie, Naohiro Browse this author | | Okuma, Yasunobu Browse this author | | Ozawa, Koichiro Browse this author | | Nomura, Yasuyuki6 Browse this author |
| Authors(alt): | 野村, 靖幸6 |
| Keywords: | Endoplasmic reticulum stress | | PI3K-Akt pathway | | Y294002 | | Wortmannin | | PD98059 | | CHOP |
| Issue Date: | Feb-2006 |
| Publisher: | Elsevier Inc. |
| Journal Title: | Biochemical and Biophysical Research Communications |
| Volume: | 340 |
| Issue: | 1 |
| Start Page: | 286 |
| End Page: | 290 |
| Publisher DOI: | 10.1016/j.bbrc.2005.12.007 |
| PMID: | 16375864 |
| Abstract: | 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. |
| Description URI: | http://www.sciencedirect.com/science/journal/0006291X |
| Type: | article (author version) |
| URI: | http://hdl.handle.net/2115/1426 |
| Appears in Collections: | 薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 野村 靖幸
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