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1996-02-26
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Document 0399
DOCN M9620399
TI Human immunodeficiency virus type 1 Vpr arrests the cell cycle in G2 by
inhibiting the activation of p34cdc2-cyclin B.
DT 9602
AU Re F; Braaten D; Franke EK; Luban J; Department of Microbiology,
Columbia University College of; Physicians and Surgeons, New York, New
YOrk 10032, USA.
SO J Virol. 1995 Nov;69(11):6859-64. Unique Identifier : AIDSLINE
MED/96013783
AB Human immunodeficiency virus type 1 (HIV-1) vpr inhibits the replication
of tumor cell lines and peripheral blood mononuclear cells. Here it is
demonstrated that expression of vpr, either in the context of a provirus
or from an independent genetic element, induces a discrete cell cycle
arrest, with cells containing 4N DNA. Low cyclin B-associated kinase
activity, as well as the status of p34cdc2 and cdc25C phosphorylation,
indicates that the cascade of reactions which drives the cell into
mitosis has not been initiated. The phosphatase inhibitor okadaic acid
releases the block, suggesting that Vpr perturbs upstream regulatorsof
the G2-M transition. These studies demonstrate that HIV-1 vpr has
profound effects on the cellular factors which control entry into
mitosis and indicate vpr's potential contribution to the cellular
pathology associated with HIV-1 infection.
DE Animal Base Sequence *Cell Cycle Cell Division Comparative Study
Cyclins/*METABOLISM DNA Primers Flow Cytometry Gene Products,
env/BIOSYNTHESIS Gene Products, vpr/*METABOLISM Genes, vpr G2 Phase
Hela Cells Human HIV Core Protein p24/BIOSYNTHESIS
HIV-1/GENETICS/*PHYSIOLOGY Mammals Molecular Sequence Data Polymerase
Chain Reaction Protein p34cdc2/*ANTAGONISTS & INHIB/METABOLISM
Support, Non-U.S. Gov't Transfection Viral Regulatory
Proteins/BIOSYNTHESIS JOURNAL ARTICLE
SOURCE: National Library of Medicine. NOTICE: This material may be
protected by Copyright Law (Title 17, U.S.Code).