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

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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
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.
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Type: article (author version)
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 野村 靖幸

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