期刊
IUBMB LIFE
卷 64, 期 10, 页码 825-834出版社
WILEY
DOI: 10.1002/iub.1078
关键词
cell signaling; innate immunity; stress; inflammation; adaptive immunity; kinase; hypoxia; DNA damage; ubiquitylation; phosphorylation
资金
- ASTAR-BMRC [07/1/22/19/523]
- NTU [RG47/10]
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
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据