Document 0161
 DOCN  M95B0161
 TI    HIV Tat represses transcription through Sp1-like elements in the basal
       promoter.
 DT    9511
 AU    Howcroft TK; Palmer LA; Brown J; Rellahan B; Kashanchi F; Brady JN;
       Singer DS; Experimental Immunology Branch, National Cancer Institute,;
       National Institutes of Health, Bethesda, MD 20892, USA.
 SO    Immunity. 1995 Jul;3(1):127-38. Unique Identifier : AIDSLINE
       MED/95346503
 AB    MHC class I genes are potently repressed by HIV Tat, which
       transactivates the HIV LTR. Tat represses class I transcription by
       binding to complexes associated with a novel promoter element,
       consisting of Sp1-like DNA binding sites. Transcription by other
       Sp1-dependent promoters, such as MDR1 and the minimal SV40 promoters, is
       also repressed by Tat, whereas the human beta-actin promoter is neither
       activated by Sp1 nor repressed by Tat. Tat repression can be overcome by
       a strong enhancer element. Thus, the SV40 72 bp enhancer element confers
       protection from Tat-mediated repression on both the minimal SV40
       promoter and the class I promoter. Surprisingly, Tat can activate the
       class I promoter in the presence of both the HIV TAR element and a
       strong upstream enhancer. These data demonstrate that Tat differentially
       affects Sp1-responsive promoters, depending on promoter architecture.
 DE    Base Sequence  Binding Sites  DNA/GENETICS  Gene Expression Regulation
       Gene Products, tat/*GENETICS  Hela Cells  Histocompatibility Antigens
       Class I/GENETICS/*IMMUNOLOGY  Human  Molecular Sequence Data  Point
       Mutation  Promoter Regions (Genetics)/GENETICS  Trans-Activation
       (Genetics)  Transcription, Genetic/GENETICS  JOURNAL ARTICLE

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