Document Detail


Dynamic disruptions in nuclear envelope architecture and integrity induced by HIV-1 Vpr.
MedLine Citation:
PMID:  11691994     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Human immunodeficiency virus-1 (HIV-1) Vpr expression halts the proliferation of human cells at or near the G2 cell-cycle checkpoint. The transition from G2 to mitosis is normally controlled by changes in the state of phosphorylation and subcellular compartmentalization of key cell-cycle regulatory proteins. In studies of the intracellular trafficking of these regulators, we unexpectedly found that wild-type Vpr, but not Vpr mutants impaired for G2 arrest, induced transient, localized herniations in the nuclear envelope (NE). These herniations were associated with defects in the nuclear lamina. Intermittently, these herniations ruptured, resulting in the mixing of nuclear and cytoplasmic components. These Vpr-induced NE changes probably contribute to the observed cell-cycle arrest.
Authors:
C M de Noronha; M P Sherman; H W Lin; M V Cavrois; R D Moir; R D Goldman; W C Greene
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Science (New York, N.Y.)     Volume:  294     ISSN:  0036-8075     ISO Abbreviation:  Science     Publication Date:  2001 Nov 
Date Detail:
Created Date:  2001-11-05     Completed Date:  2001-12-05     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0404511     Medline TA:  Science     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1105-8     Citation Subset:  IM    
Affiliation:
Gladstone Institute of Virology and Immunology, Department of Medicine, University of California, San Francisco, CA 94103, USA.
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MeSH Terms
Descriptor/Qualifier:
Active Transport, Cell Nucleus
Cell Cycle Proteins / metabolism
Cell Nucleus / metabolism*,  virology
Cyclin B / metabolism
Cyclin B1
Cytoplasm / metabolism
G2 Phase*
Gene Products, vpr / genetics,  physiology*
HIV-1 / physiology*
Hela Cells
Humans
Lamin Type B*
Lamins
Macrophages / virology
Microscopy, Fluorescence
Microscopy, Video
Mitosis
Mutation
Nuclear Envelope / metabolism*,  ultrastructure
Nuclear Pore Complex Proteins / metabolism
Nuclear Proteins / metabolism
Protein-Tyrosine Kinases / metabolism
Recombinant Fusion Proteins / metabolism
Transfection
Virus Integration
cdc25 Phosphatases / metabolism
vpr Gene Products, Human Immunodeficiency Virus
Grant Support
ID/Acronym/Agency:
KO8 AI01866/AI/NIAID NIH HHS; P30 MH59037/MH/NIMH NIH HHS; R01 AI145234/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/CCNB1 protein, human; 0/Cell Cycle Proteins; 0/Cyclin B; 0/Cyclin B1; 0/Gene Products, vpr; 0/Lamin Type B; 0/Lamins; 0/Nuclear Pore Complex Proteins; 0/Nuclear Proteins; 0/Recombinant Fusion Proteins; 0/lamin B1; 0/vpr Gene Products, Human Immunodeficiency Virus; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/WEE1 protein, human; EC 3.1.3.48/CDC25C protein, human; EC 3.1.3.48/cdc25 Phosphatases
Comments/Corrections
Comment In:
Science. 2001 Nov 2;294(5544):1016-7   [PMID:  11691977 ]
Science. 2001 Nov 2;294(5544):999   [PMID:  11695423 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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