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ID 24972
本文ファイル
著者
Hyoda, Kanae
Horie, Naohiro
Okuma, Yasunobu
Nomura, Yasuyuki
キーワード
endoplasmic reticulum stress
P13K-Akt pathway
LY294002
Wortmannin
PD98059
CHOP
NDC
医学
抄録(英)
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 MEK 1 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.
掲載誌名
Biochemical and Biophysical Research Communications
340巻
1号
開始ページ
286
終了ページ
290
出版年月日
2006-02-03
出版者
Elsevier Inc.
ISSN
0006-291X
NCID
出版者DOI
言語
英語
NII資源タイプ
学術雑誌論文
広大資料タイプ
学術雑誌論文
DCMIタイプ
text
フォーマット
application/pdf
著者版フラグ
author
権利情報
Copyright (c) 2006 Elsevier Inc.
関連情報URL(IsVersionOf)
http://dx.doi.org/10.1016/j.bbrc.2005.12.007
部局名
医歯薬学総合研究科