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      NF-kappaB antiapoptosis: induction of TRAF1 and TRAF2 and c-IAP1 and c-IAP2 to suppress caspase-8 activation.

      Science (New York, N.Y.)

      Animals, Apoptosis, Caspase 3, Caspase 8, Caspase 9, Caspases, Cysteine Endopeptidases, metabolism, Cytochrome c Group, Enzyme Activation, Etoposide, pharmacology, Gene Expression Regulation, Humans, Inhibitor of Apoptosis Proteins, Mitochondria, NF-kappa B, Proteins, genetics, physiology, Signal Transduction, TNF Receptor-Associated Factor 1, TNF Receptor-Associated Factor 2, Tumor Cells, Cultured, Tumor Necrosis Factor-alpha

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          Abstract

          Tumor necrosis factor alpha (TNF-alpha) binding to the TNF receptor (TNFR) potentially initiates apoptosis and activates the transcription factor nuclear factor kappa B (NF-kappaB), which suppresses apoptosis by an unknown mechanism. The activation of NF-kappaB was found to block the activation of caspase-8. TRAF1 (TNFR-associated factor 1), TRAF2, and the inhibitor-of-apoptosis (IAP) proteins c-IAP1 and c-IAP2 were identified as gene targets of NF-kappaB transcriptional activity. In cells in which NF-kappaB was inactive, all of these proteins were required to fully suppress TNF-induced apoptosis, whereas c-IAP1 and c-IAP2 were sufficient to suppress etoposide-induced apoptosis. Thus, NF-kappaB activates a group of gene products that function cooperatively at the earliest checkpoint to suppress TNF-alpha-mediated apoptosis and that function more distally to suppress genotoxic agent-mediated apoptosis.

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          9733516

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