Evidence map›Paper›PMID 16571786›Full record

ArticleJournal of virology2006

Induction of G2 arrest and binding to cyclophilin A are independent phenotypes of human immunodeficiency virus type 1 Vpr.

Orly Ardon, Erik S Zimmerman, Joshua L Andersen, Jason L DeHart, Jana Blackett, Vicente Planelles

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Cyclophilin A and viral infections.Biochemical and biophysical research communications · 2012
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. HIV-1 Vpr: mechanisms of G2 arrest and apoptosis.Experimental and molecular pathology · 2008
    Review
  10. Article
  11. Article
  12. 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

6 authors at 1 institution in 1 country.

Orly ArdonDivision of Cellular Biology and Immunology, Department of Pathology, University of Utah School of Medicine, 30 N 1900 East, SOM 5C210, Salt Lake City, Utah 84132, USA.
Erik S Zimmerman
Joshua L Andersen
Jason L DeHart
Jana Blackett
Vicente Planelles
University of Utah · US

Funding

TRAINING PROGRAM IN GENETICST32GM007464 · NIGMS · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., STANFIELD, GILLIAN · 1985 to 2020
$6.1M
Training Program in Microbial PathogenesisT32AI055434 · NIAID · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MULVEY, MATTHEW A, PLANELLES, VICENTE · 2004 to 2025
$6.0M
INDUCTION OF APOPTOSIS BY HIV-1 VPRR01AI049057 · NIAID · UNIVERSITY OF UTAH · PI PLANELLES, VICENTE · 2000 to 2010
$3.1M
Induction of Apoptosis by HIV-1 vprR56AI049057 · NIAID · UNIVERSITY OF UTAH · PI PLANELLES, VICENTE · 2005 to 2005
$336k
NIAID NIH HHS AI49057NIAID NIH HHS R01 AI049057NIAID NIH HHS R56 AI049057NIAID NIH HHS T32 AI055434NIGMS NIH HHS T32 GM007464NIGMS NIH HHS T32 GM07464
6 · The paper itself

Abstract

Cyclophilin A (CypA) is a member of a family of cellular proteins that share a peptidyl prolyl cis-trans isomerase (PPIase) activity. CypA was previously reported to be required for the biochemical stability and function (specifically, induction of G2 arrest) of the human immunodeficiency virus type 1 (HIV-1) protein R (Vpr). In the present study, we examine the role of the Vpr-CypA interaction on Vpr-induced G2 arrest. We find that Vpr coimmunoprecipitates with CypA and that this interaction is disrupted by substitution of proline-35 of Vpr as well as incubation with the CypA inhibitor cyclosporine A (CsA). Surprisingly, the presence of CypA or its binding to Vpr is dispensable for the ability of Vpr to induce G2 arrest. Vpr expression in CypA-/- cells leads to induction of G2 arrest in a manner that is indistinguishable from that in CypA+ cells. CsA abolished CypA-Vpr binding but had no effect on induction of G2 arrest or Vpr steady-state levels. In view of these results, we propose that the interaction with CypA is independent of the ability of Vpr to induce cell cycle arrest. The interaction between Vpr and CypA is intriguing, and further studies should examine its potential effects on other functions of Vpr.

Indexed as

G2 PhaseCell LineCyclophilin AGene Products, vprHumansPhenotypeCyclophilin AGene Products, vpr

Identifiers

PMID16571786
PMCPMC1440437
OpenAlexW2095595316

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.