Evidence map›Paper›PMID 18922870›Full record

ArticleJournal of virology2008

Human cytomegalovirus protein pp71 displaces the chromatin-associated factor ATRX from nuclear domain 10 at early stages of infection.

Vera Lukashchuk, Steven McFarlane, Roger D Everett, Chris M Preston

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 95 papers.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

95 citing papers in PubMed, 129 citations in OpenAlex.

  1. Review
  2. Review
  3. The immune response to human cytomegalovirus: impact of age, co-morbidities and the significance of anti-viral activity assessment.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Review
  4. Article
  5. Sp140L functions as a herpesvirus restriction factor suppressing viral transcription and activating interferon-stimulated genes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Remodeling of perturbed chromatin can initiate de novo transcriptional and post-transcriptional silencing.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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  11. Article
  12. Article
  13. Article
  14. Article
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  16. Review
  17. Article
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  20. Review

35 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Vera LukashchukMedical Research Council Virology Unit, Church Street, Glasgow G11 5JR, Scotland, United Kingdom.
Steven McFarlane
Roger D Everett
Chris M Preston
Medical Research Council · GB

Funding

Medical Research Council MC_U130169964Medical Research Council MC_U130169966
6 · The paper itself

Abstract

The human cytomegalovirus (HCMV) tegument protein pp71, encoded by gene UL82, stimulates viral immediate-early (IE) transcription. pp71 interacts with the cellular protein hDaxx at nuclear domain 10 (ND10) sites, resulting in the reversal of hDaxx-mediated repression of viral transcription. We demonstrate that pp71 displaces an hDaxx-binding protein, ATRX, from ND10 prior to any detectable effects on hDaxx itself and that this event contributes to the role of pp71 in alleviating repression. Introduction of pp71 into cells by transfection, infection with a pp71-expressing herpes simplex virus type 1 vector, or by generation of transformed cell lines promoted the rapid relocation of ATRX from ND10 to the nucleoplasm without alteration of hDaxx levels or localization. A pp71 mutant protein unable to interact with hDaxx did not affect the intranuclear distribution of ATRX. Infection with HCMV at a high multiplicity of infection resulted in rapid displacement of ATRX from ND10, the effect being observed maximally by 2 h after adsorption, whereas infection with the UL82-null HCMV mutant ADsubUL82 did not affect ATRX localization even at 7 h postinfection. Cell lines depleted of ATRX by transduction with shRNA-expressing lentiviruses supported increased IE gene expression and virus replication after infection with ADsubUL82, demonstrating that ATRX has a role in repressing IE transcription. The results show that ATRX, in addition to hDaxx, is a component of cellular intrinsic defenses that limit HCMV IE transcription and that displacement of ATRX from ND10 by pp71 is important for the efficient initiation of viral gene expression.

Indexed as

Adaptor Proteins, Signal TransducingCell LineCell NucleusChromatinCo-Repressor ProteinsCytomegalovirusDNA HelicasesGene DeletionGene Expression RegulationHumansMolecular ChaperonesNuclear ProteinsTime FactorsTranscription, GeneticViral ProteinsX-linked Nuclear ProteinAdaptor Proteins, Signal TransducingATRX protein, humanChromatinCo-Repressor Proteinscytomegalovirus phosphoprotein 71kDaDAXX protein, humanDNA HelicasesMolecular ChaperonesNuclear ProteinsViral ProteinsX-linked Nuclear Protein

Identifiers

PMID18922870
PMCPMC2593304
OpenAlexW2011626506

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.