       Document 0452
 DOCN  M9610452
 TI    HTLV-1 oncoprotein Tax deregulates transcription of cellular genes
       through multiple mechanisms.
 DT    9601
 AU    Yoshida M; Department of Cellular and Molecular Biology, University of;
       Tokyo, Japan.
 SO    J Cancer Res Clin Oncol. 1995;121(9-10):521-8. Unique Identifier :
       AIDSLINE MED/96034003
 AB    Infection of a human retrovirus HTLV-1 induces adult T cell leukemia and
       a neurological disease, HAM/TSP. Regulatory protein Tax of HTLV-1 is
       thought to contribute to the pathogenesis. We have studied the mechanism
       of transcriptional activation induced by Tax protein and identified two
       independent mechanisms: (a) binding to the enhancer-binding proteins,
       CREB, CREM, NF-kappa B and SRF, resulting in the activation of these
       factors through indirect binding to each specific DNA sequence, and (b)
       binding to I kappa B protein resulting in the suppression of the
       negative regulator I kappa B, which binds to NF-kappa B. In addition to
       these factors, a new protein GLI/THP is also involved in the
       transactivation. On the basis of these mechanisms, gene regulations in
       vitro and in vivo in HTLV-1-infected cells are discussed.
 DE    Base Sequence  Cell Transformation, Viral  DNA-Binding Protein, Cyclic
       AMP-Responsive/PHYSIOLOGY  DNA-Binding Proteins/PHYSIOLOGY  Enhancer
       Elements (Genetics)  Gene Expression Regulation, Viral  Gene Products,
       tax/*PHYSIOLOGY  Human  HTLV-I/*GENETICS  Molecular Sequence Data
       Nuclear Proteins/PHYSIOLOGY  NF-kappa B/PHYSIOLOGY  Proto-Oncogene
       Proteins/PHYSIOLOGY  Proto-Oncogene Proteins c-fos/PHYSIOLOGY  RNA,
       Messenger/GENETICS  Trans-Activation (Genetics)  Transcription, Genetic
       JOURNAL ARTICLE

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

