| pubmed-article:9653098 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C1704860 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9653098 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:9653098 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9653098 | pubmed:dateCreated | 1998-8-14 | lld:pubmed |
| pubmed-article:9653098 | pubmed:abstractText | By differential screening of tumor necrosis factor alpha (TNF-alpha) and lipopolysaccharide (LPS)- activated endothelial cells (ECs), we have identified a cDNA clone that turned out to be a member of the inhibitor of apoptosis (iap) gene family. iap genes function to protect cells from undergoing apoptotic death in response to a variety of stimuli. These iap genes, hiap1, hiap2, and xiap were found to be strongly upregulated upon treatment of ECs with the inflammatory cytokines TNF-alpha, interleukin 1beta, and LPS, reagents that lead to activation of the nuclear transcription factor kappaB (NF-kappaB). Indeed, overexpression of IkappaBalpha, an inhibitor of NF-kappaB, suppresses the induced expression of iap genes and sensitizes ECs to TNF-alpha-induced apoptosis. Ectopic expression of one member of the human iap genes, human X-chromosome-linked iap (xiap), using recombinant adenovirus overrules the IkappaBalpha effect and protects ECs from TNF-alpha- induced apoptosis. We conclude that xiap represents one of the NF-kappaB-regulated genes that counteracts the apoptotic signals caused by TNF-alpha and thereby prevents ECs from undergoing apoptosis during inflammation. | lld:pubmed |
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| pubmed-article:9653098 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9653098 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9653098 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9653098 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9653098 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:9653098 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:LippJJ | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:BinderB RBR | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:KumabashiriII | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:de MartinRR | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:SchaadR ERE | lld:pubmed |
| pubmed-article:9653098 | pubmed:author | pubmed-author:StehlinDD | lld:pubmed |
| pubmed-article:9653098 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9653098 | pubmed:day | 6 | lld:pubmed |
| pubmed-article:9653098 | pubmed:volume | 188 | lld:pubmed |
| pubmed-article:9653098 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9653098 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9653098 | pubmed:pagination | 211-6 | lld:pubmed |
| pubmed-article:9653098 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:9653098 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9653098 | pubmed:articleTitle | Nuclear factor (NF)-kappaB-regulated X-chromosome-linked iap gene expression protects endothelial cells from tumor necrosis factor alpha-induced apoptosis. | lld:pubmed |
| pubmed-article:9653098 | pubmed:affiliation | Department of Vascular Biology and Thrombosis Research, Vienna International Research and Cooperation Center/University of Vienna, A-1235 Vienna, Austria. | lld:pubmed |
| pubmed-article:9653098 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9653098 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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