Document 0081
 DOCN  M94A0081
 TI    Differential DNA sequence specificity and regulation of HIV-1 enhancer
       activity by cRel-RelA transcription factor.
 DT    9412
 AU    Hansen SK; Guerrini L; Blasi F; Department of Genetics and Microbiol
       Biology, University of; Milano, Italy.
 SO    J Biol Chem. 1994 Sep 2;269(35):22230-7. Unique Identifier : AIDSLINE
       MED/94350977
 AB    The cRel-RelA and NF-kappa B (p50-RelA) transcription factors bind to a
       kappa B-like sequence termed Rel-related proteins binding element
       localized in the regulatory region of the human urokinase plasminogen
       activator (uPA) gene. This sequence is highly conserved in murine and
       porcine uPA genes where it retained the ability to associate with
       cRel-RelA. On the other hand, NF-kappa B binding was obtained with the
       human and porcine elements only. Methylation interference analysis
       showed that NF-kappa B and cRel-RelA had identical interference
       patterns. Mutational analysis showed that DNA binding was highly
       sensitive to mutations within the decameric Rel-related proteins binding
       element core site. However, alterations of nucleotides flanking the
       decameric IgK-kappa B motif, which preferentially associated with
       NF-kappa B, resulted in high affinity cRel-RelA binding both in vitro
       and in vivo. These data demonstrate that NF-kappa B and cRel-RelA have
       overlapping but distinct DNA sequence specificities. Bandshift analysis
       with HeLa and Jurkat cell extracts or with in vitro translated proteins
       revealed that the SV40-, HIV-1-, and interleukin-2 receptor alpha
       subunit kappa B elements efficiently associated with cRel-RelA,
       suggesting that this heterodimer may be involved in the regulation of
       several genes. Cotransfection studies of HIV-1 long terminal
       repeat-chloramphenicol acetyltransferase reporter DNA with RelA, cRel,
       and p50 expression vectors were performed in COS7 and U293 cells to
       analyze the ability of cRel-RelA to regulate HIV-1 enhancer activity. In
       vivo formation of the cRel-RelA complex resulted in specific stimulation
       of the viral enhancer at a level comparable with that obtained with
       NF-kappa B. These data suggest that activation of cellular cRel-RelA may
       play a critical role in the regulation of HIV-1 enhancer activity.
 DE    Animal  Base Sequence  Binding Sites  DNA, Viral/*METABOLISM  *Enhancer
       Elements (Genetics)  Human  HIV Long Terminal Repeat  HIV-1/*GENETICS
       Molecular Sequence Data  NF-kappa B/*METABOLISM  Polyomavirus
       macacae/GENETICS  Support, Non-U.S. Gov't  Swine  Trans-Activation
       (Genetics)  Transcription Factors/*METABOLISM  Urokinase/GENETICS
       JOURNAL ARTICLE

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