       Document 0390
 DOCN  M9620390
 TI    A transcript from the long terminal repeats of a murine retrovirus
       associated with trans activation of cellular genes.
 DT    9602
 AU    Choi SY; Faller DV; Cancer Research Center, Boston University School of
       Medicine,; Massachusetts 02118, USA.
 SO    J Virol. 1995 Nov;69(11):7054-60. Unique Identifier : AIDSLINE
       MED/96013808
 AB    Infection of human or murine cells with murine leukemia viruses rapidly
       increases the expression of a number of genes that belong to the
       immunoglobulin superfamily and are involved in T-lymphocyte activation,
       including the class I major histocompatibility complex antigens. We have
       reported recently that the long terminal repeat (LTR) of Moloney murine
       leukemia virus encodes a trans activator which induces transcription and
       expression of class I major histocompatibility complex genes and certain
       cytokine genes. The portion of the LTR responsible for trans activation
       was mapped by deletions to lie within the U3 region. We demonstrate here
       that a transcript is initiated within the U3 region and that its
       presence correlates with the trans-activating activity. Analysis of the
       LTR region reveals a potential internal promoter element for RNA
       polymerase III transcription within the U3 region. Studies with
       polymerase inhibitors suggest that this LTR transcript, designated let
       (LTR-encoded trans activator), is a product of RNA polymerase III. The
       mechanisms whereby RNA leukemia viruses cause lymphoid neoplasia after a
       long latent period have been extensively studied but are only partially
       understood. The region of the LTR identified here as being important in
       trans activation has recently been shown to be a critical determinant of
       the leukemogenicity and latency of Moloney murine leukemia virus. These
       findings suggest a novel mechanism of retrovirus-induced activation of
       cellular gene expression, potentially contributing to leukemogenesis.
 DE    Animal  Base Sequence  Cell Line  Cell Transformation, Neoplastic
       Chloramphenicol Acetyltransferase/BIOSYNTHESIS  Genes, Viral  Human
       Mice  Mice, Inbred BALB C  Molecular Sequence Data  Moloney Leukemia
       Virus/*GENETICS/PHYSIOLOGY  Polymerase Chain Reaction  Promoter Regions
       (Genetics)  Recombinant Proteins/BIOSYNTHESIS  *Repetitive Sequences,
       Nucleic Acid  RNA Polymerase III/METABOLISM  RNA,
       Viral/BIOSYNTHESIS/ISOLATION & PURIF  Sequence Deletion  Support,
       Non-U.S. Gov't  Support, U.S. Gov't, P.H.S.  *Trans-Activation
       (Genetics)  *Transcription, Genetic  Transfection  Tumor Cells, Cultured
       Virus Latency  3T3 Cells  JOURNAL ARTICLE

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

