       Document 0119
 DOCN  M9630119
 TI    A conserved LXXLF sequence is the major determinant in p6gag required
       for the incorporation of human immunodeficiency virus type 1 Vpr.
 DT    9603
 AU    Kondo E; Gottlinger HG; Division of Human Retrovirology, Dana-Farber
       Cancer Institute,; Boston, MA 02115, USA.
 SO    J Virol. 1996 Jan;70(1):159-64. Unique Identifier : AIDSLINE
       MED/96099426
 AB    The vpr gene product of human immunodeficiency virus type (HIV-1) is a
       virion-associated regulatory protein. A transferable virion association
       motif for Vpr is located in the p6 domain of the HIV-1 Gag polyprotein.
       To map the sequences in p6 that are involved in Vpr incorporation, we
       analyzed the ability of mutant forms of p6 to direct the incorporation
       of Vpr into chimeric viral particles. Our results show that the
       determinants which govern Vpr incorporation are largely confined to a
       C-terminal region of the p6 domain. Within this region, three
       hydrophobic residues in a highly conserved sequence motif (L-X-S-L-F-G)
       are absolutely required. Remarkably, the transfer of the conserved motif
       and of a single flanking residue to a heterologous Gag polyprotein was
       sufficient to transfer the ability to incorporate Vpr at moderate
       levels. The transfer of residues 32 to 46 of p6 led to Vpr incorporation
       levels that were comparable to those obtained with full-length HIV-1 Gag
       protein, indicating that this region contains essentially all the
       information required for efficient Vpr incorporation.
 DE    Alanine  Amino Acid Sequence  Animal  Binding Sites  Carboxylic Acids
       Cell Line  *Conserved Sequence  Gene Products, gag/GENETICS/*PHYSIOLOGY
       Gene Products, vpr/*METABOLISM  Human  HIV-1/GENETICS/*PHYSIOLOGY
       Molecular Sequence Data  Peptide Fragments/PHYSIOLOGY  Support, Non-U.S.
       Gov't  Support, U.S. Gov't, P.H.S.  Virion/METABOLISM  Virus
       Assembly/PHYSIOLOGY  JOURNAL ARTICLE

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

