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

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タイトル: PI3K-Akt inactivation induced CHOP expression in endoplasmic reticulum-stressed cells
著者: Hyoda, Kanae 著作を一覧する
Hosoi, Toru 著作を一覧する
Horie, Naohiro 著作を一覧する
Okuma, Yasunobu 著作を一覧する
Ozawa, Koichiro 著作を一覧する
Nomura, Yasuyuki 著作を一覧する
キーワード: Endoplasmic reticulum stress
PI3K-Akt pathway
Y294002
Wortmannin
PD98059
CHOP
発行日: 2006年 2月
出版者: Elsevier Inc.
誌名: Biochemical and Biophysical Research Communications
巻: 340
号: 1
開始ページ: 286
終了ページ: 290
出版社 DOI: 10.1016/j.bbrc.2005.12.007
抄録: 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
資料タイプ: article (author version)
URI: http://hdl.handle.net/2115/1426
出現コレクション:雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

提供者: 野村 靖幸

 

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