Document 0080
 DOCN  M9440080
 TI    Control of the interleukin-2 promoter by the HTLV-I transactivator.
 DT    9404
 AU    Li M; City Univ. of New York, NY
 SO    Diss Abstr Int [B]; 54(4):1879 1993. Unique Identifier : AIDSLINE
       ICDB/94698005
 AB    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)
 DE    Enhancer Elements (Genetics)  Gene Deletion  Gene Expression  Gene
       Products, tax/*METABOLISM  Interleukin-2/*GENETICS  Mutation  NF-kappa
       B/METABOLISM  *Promoter Regions (Genetics)  THESIS

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