SP600125 negatively regulates the mammalian target of rapamycin via ATF4-induced Redd1 expression

被引：29

作者：

Jin, Hyeon-Ok ^{[1
]}

Seo, Sung-Keum ^{[1
]}

Woo, Sang-Hyeok ^{[1
]}

Kim, Eun-Sung ^{[1
]}

Lee, Hyung-Chahn ^{[1
]}

Yoo, Doo-Hyun ^{[1
]}

Choe, Tae-Boo ^{[2
]}

Hong, Seok-Il ^{[1
]}

Kim, Jong-Il ^{[3
]}

Park, In-Chul ^{[1
]}

机构：

[1] Korea Inst Radiol & Med Sci, Div Canc Radiat Biol, Seoul 139706, South Korea

[2] Konkuk Univ, Dept Microbiol Engn, Seoul 143701, South Korea

[3] Seoul Womens Univ, Dept Food & Microbial Technol, Seoul 139774, South Korea

来源：

FEBS LETTERS | 2009年 / 583卷 / 01期

关键词：

ATF4; JNK; Mammalian target of rapamycin; Redd1; SP600125; ACTIVATING TRANSCRIPTION FACTOR-4; CELL-CYCLE PROGRESSION; ENDOPLASMIC-RETICULUM; STRESS; PROTEIN; MTOR; HYPOXIA; PATHWAY; GROWTH; GENE;

D O I：

10.1016/j.febslet.2008.11.035

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

SP600125 (SAPK Inhibitor II) is reported to function as a reversible ATP competitive inhibitor of c-Jun N-terminal kinase (JNK). In the present study, we show that SP600125 induces a dose-dependent decrease in mTOR activity, as assessed by reduced phosphorylation of the downstream targets S6K1 and S6, and a significant increase in the expression of Redd1. Knockdown of Redd1 expression by siRNA resulted in a recovery of decreased S6 phosphorylation by SP600125. Overexpression of ATF4 upregulated the expression of Redd1, while suppression of ATF4 expression by siRNA enhanced the level of S6 phosphorylation by downregulating the SP600125-induced increase in Redd1 expression. Together, these results indicate that SP600125 inhibits mTOR activity via an ATF4-induced increase in Redd1 expression. (c) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：123 / 127

页数：5

共 44 条

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