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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5288
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pubmed:dateCreated |
1996-12-10
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pubmed:abstractText |
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.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0036-8075
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
787-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8864120-Animals,
pubmed-meshheading:8864120-Annexin A5,
pubmed-meshheading:8864120-Apoptosis,
pubmed-meshheading:8864120-Cells, Cultured,
pubmed-meshheading:8864120-DNA-Binding Proteins,
pubmed-meshheading:8864120-Feedback,
pubmed-meshheading:8864120-Humans,
pubmed-meshheading:8864120-I-kappa B Proteins,
pubmed-meshheading:8864120-Jurkat Cells,
pubmed-meshheading:8864120-Mice,
pubmed-meshheading:8864120-NF-kappa B,
pubmed-meshheading:8864120-Phosphatidylserines,
pubmed-meshheading:8864120-Signal Transduction,
pubmed-meshheading:8864120-Transcription Factor RelA,
pubmed-meshheading:8864120-Tumor Necrosis Factor-alpha
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pubmed:year |
1996
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pubmed:articleTitle |
Suppression of TNF-alpha-induced apoptosis by NF-kappaB.
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pubmed:affiliation |
Laboratory of Genetics, Salk Institute, La Jolla, CA 92037, USA. Jolla Institute for Allergy and Immu.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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