| pubmed-article:12773388 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C0664336 | lld:lifeskim |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C1425201 | lld:lifeskim |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C0178555 | lld:lifeskim |
| pubmed-article:12773388 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
| pubmed-article:12773388 | pubmed:issue | 11 | lld:pubmed |
| pubmed-article:12773388 | pubmed:dateCreated | 2003-5-29 | lld:pubmed |
| pubmed-article:12773388 | pubmed:abstractText | Survivin is an anti-apoptotic protein that is overexpressed in most human cancers. We show that survivin forms complexes with a cellular protein, hepatitis B X-interacting protein (HBXIP), which was originally recognized for its association with the X protein of hepatitis B virus (HBX). Survivin-HBXIP complexes, but neither survivin nor HBXIP individually, bind pro-caspase-9, preventing its recruitment to Apaf1, and thereby selectively suppressing apoptosis initiated via the mitochondria/cytochrome c pathway. Viral HBX protein also interacts with the survivin- HBXIP complex and suppresses caspase activation in a survivin-dependent manner. Thus, HBXIP functions as a cofactor for survivin, and serves as a link between the cellular apoptosis machinery and a viral pathogen involved in hepatocellular carcinogenesis. | lld:pubmed |
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| pubmed-article:12773388 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12773388 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12773388 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12773388 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12773388 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:12773388 | pubmed:issn | 0261-4189 | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:ArmstrongRobe... | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:ReedJohn CJC | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:MatsuzawaShu-... | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:MarusawaHiroy... | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:WelshKateK | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:TammIngoI | lld:pubmed |
| pubmed-article:12773388 | pubmed:author | pubmed-author:ZouHuaH | lld:pubmed |
| pubmed-article:12773388 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12773388 | pubmed:day | 2 | lld:pubmed |
| pubmed-article:12773388 | pubmed:volume | 22 | lld:pubmed |
| pubmed-article:12773388 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12773388 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12773388 | pubmed:pagination | 2729-40 | lld:pubmed |
| pubmed-article:12773388 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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