Abstract
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.
Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptive Immunity*
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Animals
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Cytokines / immunology
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Cytokines / metabolism
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DNA Damage / immunology
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Gene Expression Regulation / immunology*
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Humans
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Hypoxia / immunology
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Immunity, Innate*
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MAP Kinase Kinase 4 / genetics
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MAP Kinase Kinase 4 / immunology
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MAP Kinase Kinase Kinases / genetics
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MAP Kinase Kinase Kinases / immunology*
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Mice
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NF-kappa B / genetics
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NF-kappa B / immunology
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Signal Transduction / immunology*
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Toll-Like Receptors / genetics
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Toll-Like Receptors / immunology
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p38 Mitogen-Activated Protein Kinases / genetics
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p38 Mitogen-Activated Protein Kinases / immunology
Substances
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Cytokines
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NF-kappa B
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Toll-Like Receptors
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p38 Mitogen-Activated Protein Kinases
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MAP Kinase Kinase Kinases
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MAP kinase kinase kinase 7
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MAP Kinase Kinase 4