Document 0484
 DOCN  M9550484
 TI    Elements in the long terminal repeat of HIV-1 that interact with nuclear
       extracts from Jurkat cells persistently infected with vaccinia virus.
 DT    9505
 AU    Chang PY; Stellrecht K; Melana S; Pogo BG; Department of Microbiology,
       Mount Sinai School of Medicine, New; York, NY 10029.
 SO    Virus Res. 1994 Nov;34(2):127-38. Unique Identifier : AIDSLINE
       MED/95159659
 AB    Previous reports showed transactivation of the long terminal repeat
       (LTR) of HIV-1 in Jurkat cells persistently infected with vaccinia
       virus. In this communication, electrophoretic mobility shift assays were
       used to characterize the elements in HIV-1 LTR which might be
       responsible for the mechanism of transactivation. The results indicated
       that two elements, those for binding NF-kB and NFAT-1, were able to
       interact with nuclear extracts derived from Jurkat cells persistently
       infected with vaccinia virus, suggesting that they may play a role in
       the transactivation of HIV-1 LTR.
 DE    Base Sequence  Binding Sites  Binding, Competitive  Cell Line  Cell
       Nucleus/*METABOLISM  Cell Transformation, Viral  DNA-Binding
       Proteins/METABOLISM  DNA, Viral/METABOLISM  Enhancer Elements (Genetics)
       Human  *HIV Long Terminal Repeat  HIV-1/*GENETICS  Molecular Sequence
       Data  Nuclear Proteins/*METABOLISM  NF-kappa B/METABOLISM
       Oligodeoxyribonucleotides  Restriction Mapping  Substrate Specificity
       Support, Non-U.S. Gov't  *Trans-Activation (Genetics)  Transcription
       Factors/METABOLISM  Vaccinia Virus/*GENETICS  JOURNAL ARTICLE

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