Regulation of HIV-1 transcription by NF-IL6 in activated Jurkat T cells.
To examine the mechanism of HIV-1 regulation by NF-IL6 in activated human cells, we selected a Jurkat cell line that did not contain endogenous NF-IL6. In this cellular environment, we evaluated the effect of exogenous NF-IL6 on transcription mediated by native and deleted LTR sequences. In Jurkat cells stimulated with LPS and PMA, LTR-mediated transcription was enhanced by NF-IL6. The results of deletion studies revealed a central role for the basal LTR region and the TATA element in the LTR, in upregulation of reporter gene expression by NF-IL6 in activated cells. In the selected cellular environment, regulation of transcription by NF-IL6 was not evident in studies of promoter regions of other genes. The results implied that the basal region of HIV-1 LTR includes molecular properties that support activation of HIV-1 by NF-IL6 in stimulated cells.
D022782:CCAAT-Enhancer-Binding Protein-beta / Q000494:pharmacology*; D015967:Gene Expression Regulation, Viral; D016325:HIV Long Terminal Repeat / Q000235:genetics; D015497:HIV-1 / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D019169:Jurkat Cells / Q000821:virology*; D008213:Lymphocyte Activation; D011401:Promoter Regions, Genetic; D014158:Transcription, Genetic / Q000187:drug effects*
D022782:CCAAT-Enhancer-Binding Protein-beta