Mechanism of transcriptional activation of viral and cellular genes by oncogenic protein of HTLV-1 (Meeting abstract).

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Mechanism of transcriptional activation of viral and cellular genes by oncogenic protein of HTLV-1 (Meeting abstract).

International Association for Comparative Research on Leukemia and Related Diseases, 16th Symposium. July 11-16, 1993, Montreal, Quebec, Canada, A38, 1993.. Unique Identifier : AIDSLINE ICDB/94698640
Yoshida M; Dept. of Cellular and Molecular Biology, Inst. of Medical; Science, Univ. of Tokyo, Tokyo 108, Japan

Abstract: A human retrovirus, HTLV-1, is known as an etiologic agent for adult T-cell leukemia (ATL) and tropical spastic paraparesis (HAM/TSP). The regulatory gene tax appeared to enhance expression of the viral genes and also of certain cellular genes. Through the activation of some cellular genes, Tax has been proposed to contribute to abnormal proliferation of infected T cells and to production of various cytokines that are frequently associated with phenotypes of the diseases. The responsive elements for Tax transactivation have been identified as a 21-bp enhancer in the LTR, the NF-kappa B binding site of the IL-2R alpha and the CArG box of c-fos genes. It does not bind to these enhancer DNAs by its alone, thus participation of some cellular proteins has been proposed. Our previous observation using GAL-4 Tax fusion protein suggested that direct binding of the fusion protein to the DNA through GAL4 domain is required for the activation, thus, indirect association of Tax protein to the specific enhancers has been proposed. Such interaction might be mediated through enhancer binding proteins that bind to Tax protein. To identify cellular proteins contribute to the transactivation, we studied proteins that bind to the enhancer and to Tax protein. We found that leucine zipper proteins, CREB (CRE binding protein) and CREM (CRE modulator protein), do bind to Tax protein and then bind to the CRE sequence of DNA. The Tax also found to bind to a precursor p105 of the NF-kappa B. These bindings were characterized and their involvements in the transactivation mediated by Tax.

Keywords: DNA/GENETICS DNA-Binding Protein, Cyclic AMP-Responsive/GENETICS DNA-Binding Proteins/GENETICS Fungal Proteins/GENETICS Gene Products, tax/*GENETICS Genes, fos Human HIV Enhancer/GENETICS HIV Long Terminal Repeat/GENETICS Interleukin-2/METABOLISM Leucine Zippers/GENETICS NF-kappa B/GENETICS *Trans-Activation (Genetics) ABSTRACT
940830
M9480801

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