このエントリーをはてなブックマークに追加
ID 47051
本文ファイル
著者
Niinuma, Yoshifumi
Nomura, Yasuyuki
キーワード
endoplasmic reticulum (ER) stress
nuclear transcription factor-κB (NF-κB)
IRE1
TRAF2
NDC
医学
抄録(英)
Conditions that perturb the function of the endoplasmic reticulum (ER) lead to an accumulation of proteins and subsequent induction of several responses, such as an increased expression of ER-resident chaperones involved in protein folding and activation of c-jun N-terminal kinase (JNK). These responses are mediated by a transmembrane kinase/ribonuclease, IRE1, which transduces the signal from the ER lumen to the cytosol. Although nuclear transcription factor-κB (NF-κB) is also activated by ER stress, whether this response depends on IRE1 is unknown. In this study, we show that IRE1 is involved in the activation of NF-κB induced by ER stress. NF-κB was activated by ER stress-inducing agents, thapsigargin and tunicamycin. The activation was inhibited by a dominant-negative IRE1. In addition, a dominant-negative TRAF2 also suppressed the activation of NF-κB by ER stress. These results suggest that ER stress-induced NF-κB activation is also mediated by the IRE1-TRAF2 pathway, as well as JNK activation.
内容記述
The present study was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology, Japan.
掲載誌名
Biological and Pharmaceutical Bulletin
26巻
7号
開始ページ
931
終了ページ
935
出版年月日
2003-07
出版者
The Pharmaceutical Society of Japan
ISSN
0918-6158
1347-5215
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
publisher
権利情報
© 2003 Pharmaceutical Society of Japan
関連情報URL
部局名
医歯薬保健学研究科