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- W2048251436 abstract "Abstract Human T cell leukemia virus type 1 (HTLV-1), the cause of adult T cell leukemia (ATL), induces clonal expansion of infected T-cells in nonleukemic individuals and immortalizes T cells in vitro. The resistance against apoptotic stimuli of these cells hints at a viral survival function in addition to a proliferation-stimulating activity. Here we describe the up-regulation of the antiapoptotic HIAP-1/CIAP-2 gene as a consistent phenotype of HTLV-1–transformed and ATL-derived cultures and its stimulation by the viral oncoprotein Tax. Cotransfections revealed a 60-fold increase of HIAP-1 promoter activity mediated by Tax mainly via nuclear factor-κB (NF-κB) activation. To address the relevance of virally increased HIAP-1 levels for the survival of HTLV-1–transformed cells, its expression was RNA interference (RNAi) suppressed using a lentiviral transduction system. This resulted in a dramatic reduction of cell growth, a strong induction of apoptosis rates, and increased caspases 3/7 activity, which is known to be suppressed by HIAP-1. Thus, the Tax-mediated HIAP-1 overexpression is required to suppress endogenous apoptosis and, therefore, is essential for the survival of HTLV-1–transformed lymphocytes. Moreover, this points to HIAP-1 as an important target of the HTLV-1–mediated NF-κB activation." @default.
- W2048251436 created "2016-06-24" @default.
- W2048251436 creator A5003900008 @default.
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- W2048251436 creator A5058923583 @default.
- W2048251436 creator A5074241580 @default.
- W2048251436 creator A5090486832 @default.
- W2048251436 date "2006-06-01" @default.
- W2048251436 modified "2023-10-18" @default.
- W2048251436 title "Requirement of the human T-cell leukemia virus (HTLV-1) tax-stimulated HIAP-1 gene for the survival of transformed lymphocytes" @default.
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- W2048251436 doi "https://doi.org/10.1182/blood-2005-08-3138" @default.
- W2048251436 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16467195" @default.
- W2048251436 hasPublicationYear "2006" @default.
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