Evidence map›Paper›PMID 23358825›Full record

ArticleNucleic acids research2013

The Epstein-Barr virus nuclear antigen-1 reprograms transcription by mimicry of high mobility group A proteins.

Giuseppe Coppotelli, Nouman Mughal, Simone Callegari, Ramakrishna Sompallae, Laia Caja, Martijn S Luijsterburg, Nico P Dantuma, Aristidis Moustakas, Maria G Masucci

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Applying 3D Genome Technology in Virology Research.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Burkitt Lymphomas Evolve to Escape Dependencies on Epstein-Barr Virus.Frontiers in cellular and infection microbiology · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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

9 authors at 4 institutions in 2 countries.

Giuseppe CoppotelliDepartment of Cell and Molecular Biology, Karolinska Institutet, 17177 Stockholm, Sweden.
Nouman Mughal
Simone Callegari
Ramakrishna Sompallae
Laia Caja
Martijn S Luijsterburg
Nico P Dantuma
Aristidis Moustakas
Maria G Masucci
Leiden University Medical Center · NLScience for Life Laboratory · SEUppsala University · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viral proteins reprogram their host cells by hijacking regulatory components of protein networks. Here we describe a novel property of the Epstein-Barr virus (EBV) nuclear antigen-1 (EBNA1) that may underlie the capacity of the virus to promote a global remodeling of chromatin architecture and cellular transcription. We found that the expression of EBNA1 in transfected human and mouse cells is associated with decreased prevalence of heterochromatin foci, enhanced accessibility of cellular DNA to micrococcal nuclease digestion and decreased average length of nucleosome repeats, suggesting de-protection of the nucleosome linker regions. This is a direct effect of EBNA1 because targeting the viral protein to heterochromatin promotes large-scale chromatin decondensation with slow kinetics and independent of the recruitment of adenosine triphosphate-dependent chromatin remodelers. The remodeling function is mediated by a bipartite Gly-Arg rich domain of EBNA1 that resembles the AT-hook of High Mobility Group A (HMGA) architectural transcription factors. Similar to HMGAs, EBNA1 is highly mobile in interphase nuclei and promotes the mobility of linker histone H1, which counteracts chromatin condensation and alters the transcription of numerous cellular genes. Thus, by regulating chromatin compaction, EBNA1 may reset cellular transcription during infection and prime the infected cells for malignant transformation.

Indexed as

Amino Acid MotifsAnimalsAntigens, NuclearCell LineCell NucleusChromatin Assembly and DisassemblyGene Regulatory NetworksHerpesvirus 4, HumanHeterochromatinHistonesHMGA ProteinsHost-Pathogen InteractionsHumansMiceMolecular MimicryNuclear Localization SignalsAntigens, NuclearHeterochromatinHistonesHMGA ProteinsNuclear Localization SignalsViral Proteins

Identifiers

PMID23358825
PMCPMC3597695
OpenAlexW2159417180

What OpenQuestion holds

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LicenceCC BY-NC
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.