Control of the interleukin-2 promoter by the HTLV-I transactivator.
Item
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Title
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Control of the interleukin-2 promoter by the HTLV-I transactivator.
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Identifier
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AAI9325120
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identifier
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9325120
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Creator
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Li, Mian.
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Contributor
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Adviser: Miriam Siekevitz
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Date
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1993
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Language
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English
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Publisher
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City University of New York.
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Subject
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Health Sciences, Immunology | Biology, Microbiology
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Abstract
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The 40-kDa nuclear protein tax encoded by human T cell leukemia virus type I (HTLV-I) can transcriptionally activate the interleukin-2 (IL-2) enhancer and prevent inhibition of IL-2 gene expression by the immunosuppressant Cyclosporin A (CsA). We have identified a tax responsive element (TxRE) from {dollar}-{dollar}164 to {dollar}-{dollar}145 bp in the IL-2 enhancer which is sufficient to confer tax responsiveness. A 45-kDa nuclear protein (TxREF), which is expressed in Jurkat-tax cell lines but not in Jurkat cells without tax, specifically interacts with 5{dollar}\sp\prime{dollar}TxRE sequences from {dollar}-{dollar}164 to {dollar}-{dollar}154. Deletion or mutation of 5{dollar}\sp\prime{dollar}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.
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Type
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dissertation
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Source
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PQT Legacy CUNY.xlsx
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degree
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Ph.D.
