       Document 0116
 DOCN  M9550116
 TI    A novel LBP-1-mediated restriction of HIV-1 transcription at the level
       of elongation in vitro.
 DT    9505
 AU    Parada CA; Yoon JB; Roeder RG; Laboratory of Biochemistry and Molecular
       Biology, Rockefeller; University, New York, New York 10021.
 SO    J Biol Chem. 1995 Feb 3;270(5):2274-83. Unique Identifier : AIDSLINE
       MED/95138199
 AB    The cellular factor, LBP-1, can repress HIV-1 transcription by
       preventing the binding of TFIID to the promoter. Here we have analyzed
       the effect of recombinant LBP-1 on HIV-1 transcription in vitro by using
       a pulse-chase assay. LBP-1 had no effect on initiation from a preformed
       preinitiation complex and elongation to position +13 (pulse). However,
       addition of LBP-1 after RNA polymerase was stalled at +13 strongly
       inhibited further elongation (chase) by reducing RNA polymerase
       processivity. Severe mutations of the high affinity LBP-1 binding sites
       between 4 and +21 did not relieve the LBP-1-dependent block. However,
       LBP-1 could bind independently to upstream low affinity sites (-80 to
       -4), suggesting that these sites mediate the effect of LBP-1 on
       elongation. These results demonstrate a novel function of LBP-1,
       restricting HIV-1 transcription at the level of elongation. In addition,
       Tat was found to suppress the antiprocessivity effect of LBP-1 on HIV-1
       transcription in nuclear extracts. These findings strongly suggest that
       LBP-1 may provide a natural mechanism for restricting the elongation of
       HIV-1 transcripts and that this may be a target for the action of Tat in
       enhancing transcription.
 DE    Base Sequence  DNA-Binding Proteins/*PHYSIOLOGY  Gene Expression
       Regulation, Viral  Gene Products, tat/METABOLISM  Hela Cells  Human
       HIV-1/*GENETICS  In Vitro  Molecular Sequence Data  Mutagenesis,
       Site-Directed  Promoter Regions (Genetics)  Recombinant Proteins
       Repressor Proteins/*PHYSIOLOGY  RNA Polymerases/*METABOLISM  RNA,
       Viral/*BIOSYNTHESIS  Structure-Activity Relationship  Support, Non-U.S.
       Gov't  Support, U.S. Gov't, P.H.S.  Transcription, Genetic  TATA Box
       JOURNAL ARTICLE

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

