       Document 0411
 DOCN  M9620411
 TI    Interactions of the transcription factor AP-1 with the long terminal
       repeat of different human immunodeficiency virus type 1 strains in
       Jurkat, glial, and neuronal cells.
 DT    9602
 AU    Canonne-Hergaux F; Aunis D; Schaeffer E; Unite INSERM 338, Centre de
       Neurochimie, Strasbourg, France.
 SO    J Virol. 1995 Nov;69(11):6634-42. Unique Identifier : AIDSLINE
       MED/96013755
 AB    Human immunodeficiency virus type 1 (HIV-1) infection of the neuronal
       and astroglial cells of the central nervous system has been proposed to
       contribute to HIV-1-associated dementia. Recently it was shown that
       differences in the nucleotide sequence of the long terminal repeat (LTR)
       of different HIV-1 strains govern the tissue-specific pattern of viral
       expression. The LTR from central nervous system-derived HIV-1 strains
       JR-FL and JR-CSF directs expression in the neurons of transgenic mice,
       in contrast with the lymphotropic LAI strain. By in vitro footprinting,
       gel retardation, and methylation interference experiments, we have
       studied the interactions of host cell proteins from human neuronal,
       glial, HeLa, and Jurkat T cells with the LTRs from the neurotropic JR-FL
       and JR-CSF strains, compared with the LAI strain. Proteins belonging to
       the nuclear receptor family bind with different affinities to variant
       -352 to 324 sites. Gel supershift assays with Jun and Fos antibodies
       showed that the AP-1 transcription factor present in the various cell
       types was unable to recognize the -352 to -324 and -306 to 285 AP-1
       putative binding sites. Interestingly, Jun and Fos components of AP-1
       interact with the variant TGGCTCA sequence located in the -247 to -222
       region of both neurotropic strains. These interactions were cell type
       specific, since they were detected only with extracts from glial and
       HeLa cells and not from neuronal or Jurkat cells. Cotransfection
       experiments further revealed that the -247 to -222 sequence is able to
       mediate AP-1-induced transcriptional activation in glial and not
       neuronal cells.
 DE    Animal  Astrocytoma  Base Sequence  Binding Sites  Binding, Competitive
       Cell Line  Comparative Study  DNA, Viral/*METABOLISM  Hela Cells  Human
       *HIV Long Terminal Repeat  HIV-1/CLASSIFICATION/*GENETICS/METABOLISM
       Methylation  Mice  Mice, Transgenic  Molecular Sequence Data
       Neuroblastoma  Neuroglia/*METABOLISM/VIROLOGY
       Neurons/*METABOLISM/VIROLOGY  Nuclear Proteins/ISOLATION &
       PURIF/*METABOLISM  Oligodeoxyribonucleotides  Substrate Specificity
       Support, Non-U.S. Gov't  Transcription Factor AP-1/ISOLATION &
       PURIF/*METABOLISM  Tumor Cells, Cultured  Variation (Genetics)  JOURNAL
       ARTICLE

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

