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• W2115835980 abstract "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-FLIPL and c-FLIPS. 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." @default.
• W2115835980 created "2016-06-24" @default.
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• W2115835980 date "2006-05-15" @default.
• W2115835980 modified "2023-10-16" @default.
• W2115835980 title "HTLV-1 Tax protects against CD95-mediated apoptosis by induction of the cellular FLICE-inhibitory protein (c-FLIP)" @default.
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• W2115835980 doi "https://doi.org/10.1182/blood-2005-06-2567" @default.
• W2115835980 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16403915" @default.
• W2115835980 hasPublicationYear "2006" @default.
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