| pubmed-article:16403915 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0020094 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0540654 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C1413357 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0039371 | lld:lifeskim |
| pubmed-article:16403915 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:16403915 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:16403915 | pubmed:dateCreated | 2006-5-4 | lld:pubmed |
| pubmed-article:16403915 | pubmed:abstractText | The HTLV-1 transactivator protein Tax is essential for malignant transformation of CD4 T cells, ultimately leading to adult T-cell leukemia/lymphoma (ATL). Malignant transformation may involve development of apoptosis resistance. In this study we investigated the molecular mechanisms by which HTLV-1 Tax confers resistance toward CD95-mediated apoptosis. We show that Tax-expressing T-cell lines derived from HTLV-1-infected patients express elevated levels of c-FLIP(L) and c-FLIP(S). The levels of c-FLIP correlated with resistance toward CD95-mediated apoptosis. Using an inducible system we demonstrated that both resistance toward CD95-mediated apoptosis and induction of c-FLIP are dependent on Tax. In addition, analysis of early cleavage of the BH3-only Bcl-2 family member Bid, a direct caspase-8 substrate, revealed that apoptosis is inhibited at a CD95 death receptor proximal level in Tax-expressing cells. Finally, using siRNA we directly showed that c-FLIP confers Tax-mediated resistance toward CD95-mediated apoptosis. In conclusion, our data suggest an important mechanism by which expression of HTLV-1 Tax may lead to immune escape of infected T cells and, thus, to persistent infection and transformation. | lld:pubmed |
| pubmed-article:16403915 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16403915 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16403915 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16403915 | pubmed:month | May | lld:pubmed |
| pubmed-article:16403915 | pubmed:issn | 0006-4971 | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:KruegerAndrea... | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:KrammerPeter... | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:BaumannSvenS | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:Li-WeberMinM | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:HoltkotteDeni... | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:BoschValerieV | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:GiaisiMarcoM | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:MerlingAnette... | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:FasStefanie... | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:BleuminkMarcM | lld:pubmed |
| pubmed-article:16403915 | pubmed:author | pubmed-author:StumpfChristi... | lld:pubmed |
| pubmed-article:16403915 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16403915 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:16403915 | pubmed:volume | 107 | lld:pubmed |
| pubmed-article:16403915 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16403915 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16403915 | pubmed:pagination | 3933-9 | lld:pubmed |
| pubmed-article:16403915 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:16403915 | pubmed:meshHeading | pubmed-meshheading:16403915... | lld:pubmed |
| pubmed-article:16403915 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16403915 | pubmed:articleTitle | HTLV-1 Tax protects against CD95-mediated apoptosis by induction of the cellular FLICE-inhibitory protein (c-FLIP). | lld:pubmed |
| pubmed-article:16403915 | pubmed:affiliation | Tumorimmunology Program, German Cancer Research Center, Im Neuenheimer Feld 280, 69120 Heidelberg, Germany. | lld:pubmed |
| pubmed-article:16403915 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16403915 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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