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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
19
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pubmed:dateCreated |
1997-10-21
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pubmed:abstractText |
Members of the NF-kappaB/Rel and inhibitor of apoptosis (IAP) protein families have been implicated in signal transduction programs that prevent cell death elicited by the cytokine tumor necrosis factor alpha (TNF). Although NF-kappaB appears to stimulate the expression of specific protective genes, neither the identities of these genes nor the precise role of IAP proteins in this anti-apoptotic process are known. We demonstrate here that NF-kappaB is required for TNF-mediated induction of the gene encoding human c-IAP2. When overexpressed in mammalian cells, c-IAP2 activates NF-kappaB and suppresses TNF cytotoxicity. Both of these c-IAP2 activities are blocked in vivo by coexpressing a dominant form of IkappaB that is resistant to TNF-induced degradation. In contrast to wild-type c-IAP2, a mutant lacking the C-terminal RING domain inhibits NF-kappaB induction by TNF and enhances TNF killing. These findings suggest that c-IAP2 is critically involved in TNF signaling and exerts positive feedback control on NF-kappaB via an IkappaB targeting mechanism. Functional coupling of NF-kappaB and c-IAP2 during the TNF response may provide a signal amplification loop that promotes cell survival rather than death.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-1315830,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-14732063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-1589769,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2225078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2434436,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2518691,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2557547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2722778,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-2771659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-3038955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-3657593,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-6609199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7479976,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7544915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7552992,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7590248,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7667287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7739562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7769676,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7813013,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7878466,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-7957109,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8069916,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8444879,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8548810,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8548811,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8552191,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8565075,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8650213,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8654366,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8690927,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8692885,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8806678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8864118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8864119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8864120,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8892960,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8898208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-8943045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/9294162-942051
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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 |
Sep
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pubmed:issn |
0027-8424
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
16
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pubmed:volume |
94
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
10057-62
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
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pubmed:year |
1997
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pubmed:articleTitle |
Suppression of tumor necrosis factor-induced cell death by inhibitor of apoptosis c-IAP2 is under NF-kappaB control.
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pubmed:affiliation |
Howard Hughes Medical Institute, Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-0295, USA.
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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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