       Document 0372
 DOCN  M9630372
 TI    Transcriptional repression of p53 by human T-cell leukemia virus type I
       Tax protein.
 DT    9603
 AU    Uittenbogaard MN; Giebler HA; Reisman D; Nyborg JK; Department of
       Microbiology, Colorado State University, Fort; Collins 80523, USA.
 SO    J Biol Chem. 1995 Dec 1;270(48):28503-6. Unique Identifier : AIDSLINE
       MED/96081901
 AB    The human T-cell leukemia virus type I oncoprotein Tax transcriptionally
       deregulates a wide variety of viral and cellular genes. Tax deregulation
       of gene expression is mediated through interaction with a variety of
       structurally unrelated cellular transcription factors, as Tax does not
       bind DNA in a sequence-specific manner. Although most of these cellular
       transcription factors have been shown to mediate activation by Tax, we
       have recently demonstrated that members of the basic helix-loop-helix
       (bHLH) family of transcription factors, which play a critical role in
       progression through the cell cycle, mediate repression by Tax. In this
       report, we examined whether Tax might repress transcription of the tumor
       suppressor p53, as the p53 gene has recently been demonstrated to be
       regulated by the bHLH protein c-Myc. Furthermore, loss or inactivation
       of the p53 gene has been shown to be causally associated with oncogenic
       transformation. We show that Tax represses transcription of the p53 gene
       and that this repression is dependent upon the bHLH recognition element
       in the p53 promoter. Together, these results suggest that Tax may
       promote malignant transformation through repression of p53
       transcription.
 DE    Cell Line  Chloramphenicol Acetyltransferase/GENETICS  Gene Products,
       tax/*PHYSIOLOGY  *Genes, p53  Human  Promoter Regions (Genetics)
       Proto-Oncogene Proteins c-myc/PHYSIOLOGY  Support, Non-U.S. Gov't
       Support, U.S. Gov't, P.H.S.  Transcription Factors/PHYSIOLOGY
       *Transcription, Genetic  JOURNAL ARTICLE

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

