Evidence map›Paper›PMID 21526938›Full record

ArticleFuture microbiology2011

HIV-1 Vpr and G2 cell cycle arrest.

Masako Nomaguchi, Akio Adachi

Abstract readComment
PubMed Publisher
In one paragraph

Article in Future microbiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 88% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Masako NomaguchiDepartment of Microbiology, Institute of Health Biosciences, The University of Tokushima Graduate School, Kuramoto, Tokushima, Japan.
Akio Adachi
Tokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Evaluation of: Belzile J-P, Abrahamyan LG, Gerard FCA et al.: Formation of mobile chromatin-associated nuclear foci containing HIV-1 Vpr and VPRBP is critical for the induction of G2 cell cycle arrest. PLoS Pathog. 6(9), E1001080 (2010). All primate immunodeficiency viruses encode a unique set of accessory proteins to optimize their replication in hosts. In general, these proteins appear to be multifunctional for virus replication. Viral protein R (Vpr), one of the accessory proteins, has also been reported to exhibit distinct activities, but its exact role in the viral life cycle is still unclear and controversial. However, of particular note, Vpr-mediated G2 cell cycle arrest is conserved among primate immunodeficiency viruses. Belzile et al. have characterized and analyzed in detail the punctuate structures on the DNA of host cells formed by HIV-1 Vpr (Vpr nuclear foci). They demonstrate, mainly by confocal immunofluorescence analysis, that highly mobile chromatin-associated Vpr nuclear foci are critical for induction of the G2 cell cycle arrest.

Identifiers

PMID21526938
OpenAlexW2170805097

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.