pubmed-article:9294162 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0763658 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C1332415 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C1999216 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:9294162 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:9294162 | pubmed:issue | 19 | lld:pubmed |
pubmed-article:9294162 | pubmed:dateCreated | 1997-10-21 | lld:pubmed |
pubmed-article:9294162 | 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. | lld:pubmed |
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pubmed-article:9294162 | pubmed:language | eng | lld:pubmed |
pubmed-article:9294162 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9294162 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9294162 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9294162 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9294162 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9294162 | pubmed:month | Sep | lld:pubmed |
pubmed-article:9294162 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:LiuLL | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:BallardD WDW | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:MalimM HMH | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:ShiJ XJX | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:McKinseyT ATA | lld:pubmed |
pubmed-article:9294162 | pubmed:author | pubmed-author:GentryJ JJJ | lld:pubmed |
pubmed-article:9294162 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9294162 | pubmed:day | 16 | lld:pubmed |
pubmed-article:9294162 | pubmed:volume | 94 | lld:pubmed |
pubmed-article:9294162 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9294162 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9294162 | pubmed:pagination | 10057-62 | lld:pubmed |
pubmed-article:9294162 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:9294162 | pubmed:meshHeading | pubmed-meshheading:9294162-... | lld:pubmed |
pubmed-article:9294162 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9294162 | pubmed:articleTitle | Suppression of tumor necrosis factor-induced cell death by inhibitor of apoptosis c-IAP2 is under NF-kappaB control. | lld:pubmed |
pubmed-article:9294162 | pubmed:affiliation | Howard Hughes Medical Institute, Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN 37232-0295, USA. | lld:pubmed |
pubmed-article:9294162 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9294162 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9294162 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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