Abstract
Tumor necrosis factor alpha (TNF-alpha) signaling gives rise to a number of events, including activation of transcription factor NF-kappaB and programmed cell death (apoptosis). Previous studies of TNF-alpha signaling have suggested that these two events occur independently. The sensitivity and kinetics of TNF-alpha-induced apoptosis are shown to be enhanced in a number of cell types expressing a dominant-negative IkappaBalpha (IkappaBalphaM). These findings suggest that a negative feedback mechanism results from TNF-alpha signaling in which NF-kappaB activation suppresses the signals for cell death.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Annexin A5 / metabolism
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Apoptosis*
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Cells, Cultured
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DNA-Binding Proteins / genetics
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DNA-Binding Proteins / physiology
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Feedback
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Humans
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I-kappa B Proteins*
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Jurkat Cells
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Mice
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NF-KappaB Inhibitor alpha
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NF-kappa B / antagonists & inhibitors*
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NF-kappa B / physiology*
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Phosphatidylserines / metabolism
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Signal Transduction*
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Transcription Factor RelA
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Tumor Necrosis Factor-alpha / pharmacology*
Substances
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Annexin A5
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DNA-Binding Proteins
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I-kappa B Proteins
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NF-kappa B
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NFKBIA protein, human
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Nfkbia protein, mouse
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Phosphatidylserines
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Transcription Factor RelA
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Tumor Necrosis Factor-alpha
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NF-KappaB Inhibitor alpha