Document 0630 DOCN M94A0630 TI Activation of the NF-kappa-B p105 promoter by HTLV-I Tax. DT 9412 AU Lambert P; Ludford M; Deacon N; Doherty R; Macfarlane Burnet Centre for Medical Research, Fairfield,; Victoria. SO Annu Conf Australas Soc HIV Med. 1993 Oct 28-30;5:69 (abstract no. FB5). Unique Identifier : AIDSLINE ASHM5/94349025 AB The transactivator protein of HTLV-I, Tax, activates transcription not only from the HTLV-I LTR, but also from several other viral and cellular promoters. One of its targets is the LTR of HIV; HIV replication is enhanced in HTLV-I-infected cell lines, and there is increasing evidence that patients infected with both viruses show a more rapid progression to the diseased states associated with HIV infection. Activation of the HIV LTR by Tax is mediated by proteins of the NF-kappa B(NF-kappa B)/c-Rel system; there are two NF-kappa B target sites in the HIV LTR. Tax induces nuclear localization of cytoplasmic NF-kappa B/c-Rel, allowing it to bind to its target sites and activate transcription. There is also the possibility that Tax can increase the de novo synthesis of the NF-kappa B/c-Rel proteins. This seems especially likely given that at least some of them regulate their own synthesis. The gene encoding the precursor of NF-kappa B p50, p105, is one such gene. Reports vary on whether or not Tax can stimulate its promoter, and such activity may be cell type-dependent. Our preliminary results with Jurkat T cells indicated that a cotransfected Tax-expressing construct could activate a p105 promoter-CAT reporter plasmid, and we undertook further experiments to determine the mechanism for this. DE Cell Line Gene Amplification/*GENETICS Gene Expression Regulation, Viral/PHYSIOLOGY Gene Products, tax/*GENETICS Human HIV-1/GENETICS HTLV-I/*GENETICS NF-kappa B/*GENETICS Promoter Regions (Genetics)/*GENETICS Protein Precursors/*GENETICS Virus Replication/*GENETICS MEETING ABSTRACT SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).