TAK1, more than just innate immunity

被引：159

作者：

Dai, Liang ^{[1
]}

Thu, Chan Aye ^{[1
]}

Liu, Xin-Yu ^{[1
]}

Xi, Jiajia ^{[1
]}

Cheung, Peter C. F. ^{[1
]}

机构：

[1] Nanyang Technol Univ, Sch Biol Sci, Div Mol & Cell Biol, Singapore 637551, Singapore

来源：

IUBMB LIFE | 2012年 / 64卷 / 10期

关键词：

cell signaling; innate immunity; stress; inflammation; adaptive immunity; kinase; hypoxia; DNA damage; ubiquitylation; phosphorylation; NF-KAPPA-B; BETA-ACTIVATED KINASE-1; TGF-BETA; PROTEIN-KINASE; SIGNALING PATHWAY; POLYUBIQUITIN CHAINS; TAK1-BINDING PROTEIN-1; GENOTOXIC STRESS; STRUCTURAL BASIS; DNA-DAMAGE;

D O I：

10.1002/iub.1078

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：

Transforming growth factor beta-activated kinase 1 (TAK1) is a key regulator of the innate immunity and the proinflammatory signaling pathway. In response to interleukin-1, tumor necrosis factor-a, and toll-like receptor agonists, it mediates the activation of the nuclear factor ?B (NF-?B), c-Jun N-terminal kinase (JNK), and p38 pathways. In addition, TAK1 plays a central role in adaptive immunity, in which it mediates signaling from T- and B-cell receptors. This review will focus on recent developments and also examine the regulation of TAK1 in response to a diverse range of other stimuli including DNA damage, transforming growth factor-beta, Wnt, osmotic stress, and hypoxia. (c) 2012 IUBMB IUBMB Life, 2012, 64(10):825834, 2012

引用

页码：825 / 834

页数：10

共 70 条

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