Evidence map›Paper›PMID 14747563›Full record

ArticleJournal of virology2004

Epstein-Barr virus nuclear antigen 3C regulates cyclin A/p27 complexes and enhances cyclin A-dependent kinase activity.

Jason S Knight, Erle S Robertson

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 87 citations in OpenAlex.

  1. CMGC Kinases in Viral Infection and Human Disease.Pathogens (Basel, Switzerland) · 2026
    Review
  2. Review
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Virus-Induced Membrane Fusion in Neurodegenerative Disorders.Frontiers in cellular and infection microbiology · 2022
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Breaking Bad: How Viruses Subvert the Cell Cycle.Frontiers in cellular and infection microbiology · 2018
    Review
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Jason S KnightDepartment of Microbiology and Abramson Comprehensive Cancer Center, University of Pennsylvania Medical School, Philadelphia, Pennsylvania 19104, USA.
Erle S Robertson
University of Pennsylvania · US

Funding

Mechanisms of Action of LANA encoded by KSHVR01CA091792 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S. · 2002 to 2011
$3.4M
Role of EBNA3C in B Lymphocyte TransformationR01CA072150 · NCI · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S · 2002 to 2006
$1.4M
EBV Associated Head and Neck CancersR01DE014136 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI ROBERTSON, ERLE S · 2001 to 2005
$1.4M
EBNA3C AND B LYMPHOCYTE TRANSFORMATIONR29CA072150 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ROBERTSON, ERLE S · 1996 to 2000
$46k
NCI NIH HHS CA72150-07NCI NIH HHS CA91792-01NCI NIH HHS R01 CA072150NCI NIH HHS R01 CA091792NCI NIH HHS R29 CA072150NIDCR NIH HHS DE14136-01NIDCR NIH HHS R01 DE014136
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) nuclear antigen 3C (EBNA3C) is essential for primary B-cell transformation. In this report we show that cyclin A, an activator of S phase progression, bound tightly to EBNA3C. EBNA3C interacted with cyclin A in vitro and associated with cyclin A complexes in EBV-transformed lymphoblastoid cell lines. Importantly, EBNA3C stimulated cyclin A-dependent kinase activity and rescued p27-mediated inhibition of cyclin A/Cdk2 kinase activity by decreasing the molecular association between cyclin A and p27 in cells. Additionally, phosphorylation of the retinoblastoma protein, a major regulator of cell cycle progression, was enhanced both in vitro and in vivo in the presence of EBNA3C. Cyclin A interacted with a region of the carboxy terminus of EBNA3C, shown to be important both for stimulation of cyclin A-dependent kinase activity and for cell cycle progression. This provides the first evidence of an essential EBV latent antigen's directly targeting a cell cycle regulatory protein and suggests a novel mechanism by which EBV deregulates the mammalian cell cycle, which is of critical importance in B-cell transformation.

Indexed as

Cell Transformation, ViralGene Expression RegulationAntigens, ViralB-LymphocytesCell Cycle ProteinsCell Line, TransformedCell NucleusCyclin ACyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesEpstein-Barr Virus Nuclear AntigensHeLa CellsHumansTumor Suppressor ProteinsTwo-Hybrid System TechniquesAntigens, ViralCell Cycle ProteinsCyclin ACyclin-Dependent Kinase Inhibitor p27Cyclin-Dependent KinasesEBNA-3C, epstein-barr virusEpstein-Barr Virus Nuclear AntigensTumor Suppressor Proteins

Identifiers

PMID14747563
PMCPMC369513
OpenAlexW2090619917

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.