TAK1, more than just innate immunity

• Published in: IUBMB life 2012-10, Vol.64 (10), p.825-834
• Main Authors: Dai, Liang, Aye Thu, Chan, Liu, Xin‐Yu, Xi, Jiajia, Cheung, Peter C. F.
• Format: Article
• Language: English
• Subjects: Adaptive Immunity; Animals; cell signaling; Cytokines - immunology; Cytokines - metabolism; DNA damage; DNA Damage - immunology; Gene Expression Regulation - immunology; Humans; hypoxia; Hypoxia - immunology; Immunity, Innate; inflammation; innate immunity; kinase; MAP Kinase Kinase 4 - genetics; MAP Kinase Kinase 4 - immunology; MAP Kinase Kinase Kinases - genetics; MAP Kinase Kinase Kinases - immunology; Mice; NF-kappa B - genetics; NF-kappa B - immunology; p38 Mitogen-Activated Protein Kinases - genetics; p38 Mitogen-Activated Protein Kinases - immunology; phosphorylation; Signal Transduction - immunology; stress; Toll-Like Receptors - genetics; Toll-Like Receptors - immunology; ubiquitylation
• ISSN: 1521-6543; 1521-6551
• DOI: 10.1002/iub.1078

Transforming growth factor β‐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‐α, and toll‐like receptor agonists, it mediates the activation of the nuclear factor κB (NF‐κB), 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‐β, Wnt, osmotic stress, and hypoxia. © 2012 IUBMB IUBMB Life, 2012, 64(10):825–834, 2012