       Document 0097
 DOCN  M9460097
 TI    The human immunodeficiency virus type 1 Tat protein transactivates tumor
       necrosis factor beta gene expression through a TAR-like structure.
 DT    9404
 AU    Buonaguro L; Buonaguro FM; Giraldo G; Ensoli B; Laboratory of Tumor Cell
       Biology, National Cancer Institute,; National Institutes of Health,
       Bethesda, Maryland 20892.
 SO    J Virol. 1994 Apr;68(4):2677-82. Unique Identifier : AIDSLINE
       MED/94187109
 AB    We have previously shown that the Tat protein of human immunodeficiency
       virus type 1 (HIV-1) transactivates tumor necrosis factor alpha and beta
       (TNF alpha and TNF beta) gene expression in HIV-1-infected and in
       tat-transfected T-lymphocytic and monocytic cell lines. The product
       encoded by the first exon of the tat gene (amino acids 1 to 72) is
       sufficient for this transactivation. Here we show that (i) the NF-kappa
       B and Sp1 binding sites of the TNF beta promoter are required for
       Tat-mediated transactivation and (ii) a predicted stem-loop structure in
       the TNF beta mRNA leader region, which resembles the Tat-responsive
       element of the HIV-1 long terminal repeat (TAR) and which is therefore
       termed TAR-like, is essential for TNF beta transactivation by Tat. These
       data suggest that similar promoter regulatory elements are necessary for
       Tat-mediated transactivation of both TNF beta and HIV-1 gene expression.
       This represents the first demonstration of a cellular gene with a
       regulatory element downstream of the transcriptional initiation site
       that, like TAR, may function as an RNA element.
 DE    Base Sequence  Gene Expression Regulation  Gene Products,
       tat/*PHARMACOLOGY  Gene Products, tax/PHARMACOLOGY  Human
       HIV-1/*GENETICS  Lymphotoxin/BIOSYNTHESIS/*GENETICS  Molecular Sequence
       Data  Promoter Regions (Genetics)/*GENETICS  Sequence Analysis, DNA
       Support, Non-U.S. Gov't  Tetradecanoylphorbol Acetate/PHARMACOLOGY
       Trans-Activation (Genetics)/*DRUG EFFECTS  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

