Abstract
Tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine, exerts its biological activity by signaling via its two receptors, TNF-RI and TNF-RII, and by activating NF-kappaB. NF-kappaB is essential for survival of many cell types; however, TNF-alpha also induces cell death. In this article, both the survival and cell death signaling by TNF-alpha and the role of caspases in turning off NF-kappaB survival signal are reviewed. Furthermore, a role of DAP kinase in TNF-induced apoptosis is discussed. Finally, the molecular basis of the effect of age on TNF-alpha-induced apoptosis in human T cells is reviewed.
Publication types
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Aging / immunology
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Antigens, CD / metabolism
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Apoptosis / immunology*
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Apoptosis / physiology
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Apoptosis Regulatory Proteins
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism
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Caspases / metabolism
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Cell Survival / immunology*
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Cell Survival / physiology
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Death-Associated Protein Kinases
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Humans
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Mitochondria / immunology
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Mitochondria / metabolism
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Models, Immunological
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NF-kappa B / metabolism
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Receptors, Tumor Necrosis Factor / metabolism
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Receptors, Tumor Necrosis Factor, Type I
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Receptors, Tumor Necrosis Factor, Type II
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Signal Transduction
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Tumor Necrosis Factor-alpha / metabolism*
Substances
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Antigens, CD
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Apoptosis Regulatory Proteins
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NF-kappa B
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Receptors, Tumor Necrosis Factor
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Receptors, Tumor Necrosis Factor, Type I
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Receptors, Tumor Necrosis Factor, Type II
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Tumor Necrosis Factor-alpha
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Death-Associated Protein Kinases
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Calcium-Calmodulin-Dependent Protein Kinases
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Caspases