Evidence map›Paper›PMID 20810723›Full record

ArticleJournal of virology2010

Epstein-Barr Virus SM protein utilizes cellular splicing factor SRp20 to mediate alternative splicing.

Dinesh Verma, Swarna Bais, Melusine Gaillard, Sankar Swaminathan

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
1.7field-weighted citation impact, top 14% 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

47 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Macrophage Zc3h12c Limits Tissue Inflammation and Injury via Alternative Splicing of Pre-mRNA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Viral Modulation of Host Splicing.Annual review of virology · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023
    Review
  17. Article
  18. Review
  19. Review
  20. Review
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.

Dinesh VermaDepartment of Medicine, University of Florida, Gainesville, FL 32610, USA.
Swarna Bais
Melusine Gaillard
Sankar Swaminathan
University of Florida Health · US

Funding

POSTTRANSCRIPTIONAL GENE REGULATION BY EBV SM PROTEINR01CA081133 · NCI · UNIVERSITY OF UTAH · PI SWAMINATHAN, SANKAR · 1999 to 2022
$4.9M
Viral and cellular gene regulation during lytic KSHV replicationR01CA119905 · NCI · UNIVERSITY OF UTAH · PI SWAMINATHAN, SANKAR · 2006 to 2010
$1.1M
NCI NIH HHS R01 CA081133NCI NIH HHS R01 CA119905NCI NIH HHS R01 CA81133
6 · The paper itself

Abstract

Epstein-Barr virus (EBV) SM protein is an essential nuclear protein produced during the lytic cycle of EBV replication. SM is an RNA-binding protein with multiple mechanisms of action. SM enhances the expression of EBV genes by stabilizing mRNA and facilitating nuclear export. SM also influences splicing of both EBV and cellular pre-mRNAs. SM modulates splice site selection of the host cell STAT1 pre-mRNA, directing utilization of a novel 5' splice site that is used only in the presence of SM. SM activates splicing in the manner of SR proteins but does not contain the canonical RS domains typical of cellular splicing factors. Affinity purification and mass spectrometry of SM complexes from SM-transfected cells led to the identification of the cellular SR splicing factor SRp20 as an SM-interacting protein. The regions of SM and SRp20 required for interaction were mapped by in vitro and in vivo assays. The SRp20 interaction was shown to be important for the effects of SM on alternative splicing by the use of STAT1 splicing assays. Overexpression of SRp20 enhanced SM-mediated alternative splicing and knockdown of SRp20 inhibited the SM effect on splicing. These data suggest a model whereby SM, a viral protein, recruits and co-opts the function of cellular SRp20 in alternative splicing.

Indexed as

Alternative SplicingGene Expression Regulation, ViralCell LineEpstein-Barr Virus InfectionsHeLa CellsHerpesvirus 4, HumanHumansImmediate-Early ProteinsProtein BindingRNA-Binding ProteinsSerine-Arginine Splicing FactorsTrans-ActivatorsBRLF1 protein, Human herpesvirus 4Immediate-Early ProteinsRNA-Binding ProteinsSerine-Arginine Splicing FactorsSRSF3 protein, humanTrans-Activators

Identifiers

PMID20810723
PMCPMC2977868
OpenAlexW2147198871

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.