Document 0287
 DOCN  M94A0287
 TI    Human T-cell leukemia virus type I Tax protein represses gene expression
       through the basic helix-loop-helix family of transcription factors.
 DT    9412
 AU    Uittenbogaard MN; Armstrong AP; Chiaramello A; Nyborg JK; Department of
       Microbiology, Colorado State University, Fort; Collins 80523.
 SO    J Biol Chem. 1994 Sep 9;269(36):22466-9. Unique Identifier : AIDSLINE
       MED/94357879
 AB    The human T-cell leukemia virus type I (HTLV-I) oncoprotein Tax is a
       potent activator of viral and cellular gene transcription. Tax does not
       bind DNA directly but utilizes cellular transcription factors to mediate
       activation. In this report, we examine the role of the basic
       helix-loop-helix (bHLH) proteins in Tax deregulation of gene expression,
       as these proteins play a critical role in progression through the cell
       cycle and have been implicated in neoplastic disease. We show that the
       bHLH proteins do not mediate activation, but instead mediate repression
       of gene expression in the presence of Tax. We further show that a
       consensus bHLH binding site in the promoter of the beta-polymerase gene,
       which encodes an enzyme involved in DNA repair, mediates the previously
       reported repression of beta-polymerase gene expression by Tax. Together,
       these results suggest that Tax may induce malignant transformation, at
       least in part, through bHLH-mediated repression of key cellular
       regulatory genes.
 DE    Animal  Base Sequence  Binding Sites  Cell Line  Cercopithecus aethiops
       Chloramphenicol Acetyltransferase/BIOSYNTHESIS  Consensus Sequence
       DNA-Binding Proteins/*METABOLISM  *Gene Expression Regulation, Viral
       Gene Products, tax/*METABOLISM  *Helix-Loop-Helix Motifs
       HTLV-I/GENETICS/*METABOLISM  Kinetics  Molecular Sequence Data
       Oligodeoxyribonucleotides  Plasmids  Support, Non-U.S. Gov't  Support,
       U.S. Gov't, P.H.S.  Transcription Factors/*METABOLISM  Transfection
       JOURNAL ARTICLE

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