Control of the interleukin-2 promoter by the HTLV-I transactivator.

Important note: Information in this article was accurate in 1994. The state of the art may have changed since the publication date.

Control of the interleukin-2 promoter by the HTLV-I transactivator.

Diss Abstr Int [B]; 54(4):1879 1993. Unique Identifier : AIDSLINE ICDB/94698005
Li M; City Univ. of New York, NY

Abstract: The 40-kD nuclear protein tax encoded by human T cell leukemia virus type I can transcriptionally activate the interleukin-2 (IL-2) enhancer and prevent inhibition of IL-2 gene expression by the immunosuppressant cyclosporin A. We have identified a tax responsive element (TxRE) from -164 to -145 bp in the IL-2 enhancer which is sufficient to confer tax responsiveness. A 45-kD nuclear protein (TxREF), which is expressed in Jurkat-tax cell lines but not in Jurkat cells without tax, specifically interacts with 5'TxRE sequences from -164 to -154. Deletion or mutation of 5'TxRE removes the binding of TxREF in vitro and dramatically reduces tax activity in vivo. Although the TxREF binding site contains an NF-kB-like motif, TxREF is distinct from NF-kB. While the TxRE and NF-kB sites contribute to tax plus PMA inducibility of the IL-2 enhancer, the TxRE and NFAT sites are the important sites contributing to the synergistic effect of tax plus PHA inducibility of the IL-2 enhancer. These results demonstrate that TxREF is a novel tax inducible DNA binding protein and that TxRE plays a crucial role in mediating tax induced IL-2 gene expression. (Full text available from University Microfilms International, Ann Arbor, MI, as Order No. AAD93-25120)

Keywords: Enhancer Elements (Genetics) Gene Deletion Gene Expression Gene Products, tax/*METABOLISM Interleukin-2/*GENETICS Mutation NF-kappa B/METABOLISM *Promoter Regions (Genetics) THESIS
940530
M9450897

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