Document 0448
 DOCN  M9590448
 TI    Reciprocal modulations between p53 and Tat of human immunodeficiency
       virus type 1.
 DT    9509
 AU    Li CJ; Wang C; Friedman DJ; Pardee AB; Division of Cell Growth and
       Regulation, Dana-Farber Cancer; Institute, Harvard Medical School,
       Boston, MA 02115, USA.
 SO    Proc Natl Acad Sci U S A. 1995 Jun 6;92(12):5461-4. Unique Identifier :
       AIDSLINE MED/95296330
 AB    Infection by human immunodeficiency virus type 1 (HIV-1) causes acquired
       immunodeficiency syndrome (AIDS) after a long clinical latency. This
       disease is associated with a spectrum of cancers. Here we report that
       wild-type p53 is a potent suppressor of Tat, a major transactivator of
       HIV-1. Reciprocally, Tat inhibits the transcription of p53.
       Downregulation of p53 by upregulated tat may be important for the
       establishment of productive viral infection in a cell and also may be
       involved in the development of AIDS-related malignancies.
 DE    Base Sequence  Down-Regulation (Physiology)  DNA, Complementary  Gene
       Products, tat/GENETICS/*PHYSIOLOGY  Genes, p53  Genes, tat  Human  HIV
       Long Terminal Repeat  HIV-1/*GENETICS  Molecular Sequence Data  Promoter
       Regions (Genetics)  Protein p53/GENETICS/*PHYSIOLOGY  Support, U.S.
       Gov't, P.H.S.  Trans-Activation (Genetics)  Tumor Cells, Cultured  Tumor
       Necrosis Factor/PHYSIOLOGY  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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