TAK1-mediated transcriptional activation of CD28-responsive element and AP-1-binding site within the IL-2 promoter in Jurkat T cells

被引：6

作者：

Sakurai, H ^{[1
]}

Singhirunnusorn, P

Shimotabira, E

Chino, A

Suzuki, S

Koizumi, K

Saiki, I

机构：

[1] Toyama Med & Pharmaceut Univ, Div Pathogen Biochem, Inst Nat Med, Toyama 9300194, Japan

[2] Toyama Med & Pharmaceut Univ, Div Pathogen Biochem, Century COE Program 21, Toyama 9300194, Japan

[3] Toyama Med & Pharmaceut Univ, Fac Med, Dept Japanese Oriental Med, Toyama 9300194, Japan

来源：

FEBS LETTERS | 2005年 / 579卷 / 29期

关键词：

TAK1; TAB1; IL-2; T cell;

D O I：

10.1016/j.febslet.2005.10.059

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 [生物化学与分子生物学]; 081704 [应用化学];

摘要：

We focused on the functional involvement of transforming growth factor-beta-activated kinase 1 (TAK1) in transcriptional regulation of interleukin-2 (IL-2) in T cells. Costimulation of Jurkat cells with 12-O-tetradecanoylphorbol-13-acetate and A23187 leads to a rapid phosphorylation of TAK1 and TAK1-binding protein I (TAB1), critical for TAK1 activation. A specific inhibitor of TAK1 blocked production of IL-2. In addition, overexpression of TAK1 and TAB1 induced secretion of IL-2. CD28-responsive element/activator protein-1-binding site (RE/AP) within the IL-2 promoter was a functional target for TAK1. The RE/AP-driven transcription was regulated by TAK1-mediated activation of the c-Jun NH2-terminal kinase, p38 and I kappa B kinase. These results indicate that TAK1 plays a critical role in T cell activation by controlling production of IL-2. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：6641 / 6646

页数：6

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