Evidence map›Paper›PMID 18385244›Full record

ArticleJournal of virology2008

Human immunodeficiency virus type 1 Vpr binds to the N lobe of the Wee1 kinase domain and enhances kinase activity for CDC2.

Masakazu Kamata, Nobumoto Watanabe, Yoshiko Nagaoka, Irvin S Y Chen

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018
    Review
  5. Yeast for virus research.Microbial cell (Graz, Austria) · 2017
    Review
  6. HIV-1 Vpr-a still "enigmatic multitasker".Frontiers in microbiology · 2014
    Review
  7. Cell cycle regulation during viral infection.Methods in molecular biology (Clifton, N.J.) · 2014
    Review
  8. Article
  9. Vpr-host interactions during HIV-1 viral life cycle.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2011
    Review
  10. Article
  11. Article
  12. Review
  13. 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 2 institutions in 2 countries.

Masakazu KamataDepartment of Microbiology, Immunology and Molecular Genetics, University of California at Los Angeles, David Geffen School of Medicine, 615 Charles E. Young Dr. South, BSRB 173, Los Angeles, CA 90095, USA.
Nobumoto Watanabe
Yoshiko Nagaoka
Irvin S Y Chen
University of California, Los Angeles · USRIKEN Advanced Science Institute · JP

Funding

HIV 1 VPR INDUCES G2 CELL CYCLE ARREST AND APOPTOSISR01CA070018 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHEN, IRVIN S.Y. · 1995 to 2007
$2.5M
NCI NIH HHS CA070018-13NCI NIH HHS R01 CA070018NIAID NIH HHS AI1028697-18
6 · The paper itself

Abstract

Human immunodeficiency virus type 1 Vpr is a virion-associated accessory protein that has multiple activities within an infected cell. One of the most dramatic effects of Vpr is the induction of cell cycle arrest at the G(2)/M boundary, followed by apoptosis. This effect has implications for CD4(+) cell loss in AIDS. In normal cell cycle regulation, Wee1, a key regulator for G(2)-M progression, phosphorylates Tyr15 on Cdc2 and thereby blocks the progression of cells into M phase. We demonstrate that Vpr physically interacts with Wee1 at the N lobe of the kinase domain analogous to that present in other kinases. This interaction with Vpr enhances Wee1 kinase activity for Cdc2. Overexpression of Wee1 kinase-deficient mutants competes for Vpr-mediated cell cycle arrest, and deletion of the region of Wee1 that binds Vpr abrogates that competition. However, the Vpr mutants I74P and I81P, which fail to induce G(2) arrest, can bind to and increase the kinase activity of Wee1 to the same extent as wild-type Vpr. Therefore, we conclude that the binding of Vpr to Wee1 is not sufficient for Vpr to activate the G(2) checkpoint, and it may reflect an independent function of Vpr.

Indexed as

HIV-1CDC2 Protein KinaseCell Cycle ProteinsCell LineG2 PhaseGene Products, vprGlutathione TransferaseHeLa CellsHumansKidneyNuclear ProteinsPlasmidsProtein Structure, TertiaryProtein-Tyrosine KinasesRecombinant Fusion ProteinsTransfectionCDC2 Protein KinaseCell Cycle ProteinsGene Products, vprGlutathione TransferaseNuclear ProteinsProtein-Tyrosine KinasesRecombinant Fusion ProteinsWEE1 protein, human

Identifiers

PMID18385244
PMCPMC2395134
OpenAlexW2149794096

What OpenQuestion holds

Textmetadata
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.