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).