Evidence map›Paper›PMID 20609246›Full record

ArticleRetrovirology2010

Cell cycle G2/M arrest through an S phase-dependent mechanism by HIV-1 viral protein R.

Ge Li, Hyeon U Park, Dong Liang, Richard Y Zhao

Open access · goldAbstract read
In one paragraph

Article in Retrovirology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.2field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

40 citing papers in PubMed, 51 citations in OpenAlex.

  1. Manipulation of the cell cycle by HIV-1.Biochemical Society transactions · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. The HIV-1Viruses · 2024
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018
    Review
  14. Yeast for virus research.Microbial cell (Graz, Austria) · 2017
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Ge LiDepartment of Pathology, Institute of Human Virology, University of Maryland School of Medicine, Baltimore, MD, USA.
Hyeon U Park
Dong Liang
Richard Y Zhao
Georgetown University Medical Center · USIcahn School of Medicine at Mount Sinai · USUniversity of Maryland, Baltimore · US

Funding

Effect of HIV-1 Vpr on Basic Cellular Functions (II)R01AI040891 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHAO, RICHARD YUQI · 2003 to 2007
$1.4M
Cell Cycle G2/M Pathway Modulated by Viral Protein RR01GM063080 · NIGMS · UNIVERSITY OF MARYLAND BALTIMORE · PI ZHAO, RICHARD YUQI · 2002 to 2006
$968k
Effect of HIV-1 Vpr on Basic Cellular FunctionsR21AI040891 · NIAID · CHILDREN'S MEMORIAL HOSPITAL (CHICAGO) · PI ZHAO, RICHARD YUQI · 2002 to 2002
$249k
HIV-1 VPR AND BASIC CELLULAR FUNCTIONSR29AI040891 · NIAID · CHILDREN'S MEMORIAL HOSPITAL (CHICAGO) · PI ZHAO, RICHARD YUQI · 1997 to 2001
$209k
NIAID NIH HHS AI40891NIGMS NIH HHS GM63080
6 · The paper itself

Abstract

backgroundCell cycle G2 arrest induced by HIV-1 Vpr is thought to benefit viral proliferation by providing an optimized cellular environment for viral replication and by skipping host immune responses. Even though Vpr-induced G2 arrest has been studied extensively, how Vpr triggers G2 arrest remains elusive.

resultsTo examine this initiation event, we measured the Vpr effect over a single cell cycle. We found that even though Vpr stops the cell cycle at the G2/M phase, but the initiation event actually occurs in the S phase of the cell cycle. Specifically, Vpr triggers activation of Chk1 through Ser345 phosphorylation in an S phase-dependent manner. The S phase-dependent requirement of Chk1-Ser345 phosphorylation by Vpr was confirmed by siRNA gene silencing and site-directed mutagenesis. Moreover, downregulation of DNA replication licensing factors Cdt1 by siRNA significantly reduced Vpr-induced Chk1-Ser345 phosphorylation and G2 arrest. Even though hydroxyurea (HU) and ultraviolet light (UV) also induce Chk1-Ser345 phosphorylation in S phase under the same conditions, neither HU nor UV-treated cells were able to pass through S phase, whereas vpr-expressing cells completed S phase and stopped at the G2/M boundary. Furthermore, unlike HU/UV, Vpr promotes Chk1- and proteasome-mediated protein degradations of Cdc25B/C for G2 induction; in contrast, Vpr had little or no effect on Cdc25A protein degradation normally mediated by HU/UV.

conclusionsThese data suggest that Vpr induces cell cycle G2 arrest through a unique molecular mechanism that regulates host cell cycle regulation in an S-phase dependent fashion.

Indexed as

Cell DivisionG2 PhaseS Phasecdc25 PhosphatasesCell Cycle ProteinsCheckpoint Kinase 1Gene SilencingHeLa CellsHIV-1HumansMutagenesis, Site-DirectedPhosphorylationProtein KinasesVirulence Factorsvpr Gene Products, Human Immunodeficiency VirusCDC25A protein, humanCDC25B protein, humanCDC25C protein, humancdc25 PhosphatasesCDT1 protein, humanCell Cycle ProteinsCheckpoint Kinase 1CHEK1 protein, humanProtein KinasesVirulence Factorsvpr Gene Products, Human Immunodeficiency Virusvpr protein, Human immunodeficiency virus 1

Identifiers

PMID20609246
PMCPMC2909154
OpenAlexW2108667794

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.