Document 0252
 DOCN  M9550252
 TI    Intrinsic activity of human immunodeficiency virus type 1 protease
       heterologous fusion proteins in mammalian cells.
 DT    9505
 AU    Arrigo SJ; Haines JK; Huffman KM; Department of Microbiology and
       Immunology, Medical University of; South Carolina, Charleston
       29425-2230.
 SO    DNA Cell Biol. 1995 Jan;14(1):15-23. Unique Identifier : AIDSLINE
       MED/95134352
 AB    We have generated various mammalian expression constructs that produce
       fusion proteins of human immunodeficiency virus type 1 (HIV-1) protease
       (PR) with the HIV-1 Nef protein. The expression of these proteins is
       inducible by the HIV-1 Tat protein. High-level expression of
       proteolytically active PR was produced from PR imbedded into Nef coding
       sequences, flanked by PR cleavage sites. The fusion protein was cleaved
       nearly to completion and did not exhibit the regulated processing that
       is seen with the virally encoded PR. No cytotoxic effect of PR
       expression was detected. The self-cleavage of PR could be inhibited by a
       specific inhibitor of HIV-1 PR (U75875). Elimination of the
       aminoterminal PR cleavage site did not have a measurable effect on
       cleavage of the precursor fusion protein. The cleaved fusion proteins
       appeared to be extremely unstable in the transfected cells. These
       findings demonstrate the intrinsic activity of HIV-1 PR in mammalian
       cells, in the context of a heterologous fusion protein.
 DE    Animal  Base Sequence  Cell Line  Gene Expression Regulation, Viral
       Gene Products, nef/*GENETICS  Gene Products, tat/GENETICS  Genetic
       Vectors/GENETICS  Human  HIV Protease/BIOSYNTHESIS/GENETICS/*METABOLISM
       HIV Protease Inhibitors/PHARMACOLOGY  HIV-1/*METABOLISM  Mammals
       Molecular Sequence Data  Protein Processing, Post-Translational/DRUG
       EFFECTS  Recombinant Fusion Proteins/BIOSYNTHESIS/METABOLISM/TOXICITY
       RNA, Messenger/BIOSYNTHESIS  Sequence Deletion/PHYSIOLOGY  Support, U.S.
       Gov't, P.H.S.  JOURNAL ARTICLE

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