Evidence map›Paper›PMID 37410772›Full record

ArticlePLoS pathogens2023

Changes in SUMO-modified proteins in Epstein-Barr virus infection identifies reciprocal regulation of TRIM24/28/33 complexes and the lytic switch BZLF1.

Carlos F De La Cruz-Herrera, Michael H Tatham, Umama Z Siddiqi, Kathy Shire, Edyta Marcon, Jack F Greenblatt, Ronald T Hay, Lori Frappier

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Review
  2. Lactate-induced miR-7-5p/TRIM33 reprograms metabolic flux to suppress tumor growth and viral reactivation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  3. A Landscape Analysis of Human SUMOylation.Molecular & cellular proteomics : MCP · 2026
    Article
  4. Review
  5. The Pathology of Viral Infections.Advances in experimental medicine and biology · 2026
    Review
  6. Article
  7. Article
  8. Insights into the protein domains of C-VI TRIM subfamily in viral infection.Frontiers in cellular and infection microbiology · 2025
    Review
  9. KAP1 in antiviral immunity: dual roles in viral silencing and immune regulation.Frontiers in cellular and infection microbiology · 2025
    Review
  10. Review
  11. 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

8 authors at 2 institutions in 2 countries.

Carlos F De La Cruz-HerreraDepartment of Molecular Genetics, University of Toronto, Toronto, Canada.
Michael H TathamDivision of Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee, United Kingdom.
Umama Z SiddiqiDepartment of Molecular Genetics, University of Toronto, Toronto, Canada.
Kathy ShireDepartment of Molecular Genetics, University of Toronto, Toronto, Canada.
Edyta MarconDonnelly Centre, University of Toronto, Toronto, Canada.
Jack F GreenblattDepartment of Molecular Genetics, University of Toronto, Toronto, Canada.
Ronald T HayDivision of Gene Regulation and Expression, School of Life Sciences, University of Dundee, Dundee, United Kingdom.
Lori FrappierDepartment of Molecular Genetics, University of Toronto, Toronto, Canada.ORCID 0000-0003-0110-5472
University of Toronto · CAUniversity of Dundee · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

SUMO modifications regulate the function of many proteins and are important in controlling herpesvirus infections. We performed a site-specific proteomic analysis of SUMO1- and SUMO2-modified proteins in Epstein-Barr virus (EBV) latent and lytic infection to identify proteins that change in SUMO modification status in response to EBV reactivation. Major changes were identified in all three components of the TRIM24/TRIM28/TRIM33 complex, with TRIM24 being rapidly degraded and TRIM33 being phosphorylated and SUMOylated in response to EBV lytic infection. Further experiments revealed TRIM24 and TRIM33 repress expression of the EBV BZLF1 lytic switch gene, suppressing EBV reactivation. However, BZLF1 was shown to interact with TRIM24 and TRIM33, resulting in disruption of TRIM24/TRIM28/TRIM33 complexes, degradation of TRIM24 and modification followed by degradation of TRIM33. Therefore, we have identified TRIM24 and TRIM33 as cellular antiviral defence factors against EBV lytic infection and established the mechanism by which BZLF1 disables this defence.

Indexed as

Epstein-Barr Virus InfectionsCarrier ProteinsHerpesvirus 4, HumanHumansProteomicsSmall Ubiquitin-Related Modifier ProteinsTrans-ActivatorsTranscription FactorsVirus ActivationVirus LatencyBZLF1 protein, Herpesvirus 4, HumanCarrier ProteinsSmall Ubiquitin-Related Modifier ProteinsTrans-ActivatorsTranscription FactorsTRIM24 protein, humanTRIM33 protein, human

Identifiers

PMID37410772
PMCPMC10353822
OpenAlexW4383314039

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.