Evidence map›Paper›PMID 32727874›Full record

ArticleJournal of virology2020

Murine Cytomegalovirus M25 Proteins Sequester the Tumor Suppressor Protein p53 in Nuclear Accumulations.

Ivana Kutle, Katarzyna M Szymańska-de Wijs, Boris Bogdanow, Berislav Cuvalo, Lars Steinbrück, Stipan Jonjić, Karen Wagner, Rainer Niedenthal, Matthias Selbach, Lüder Wiebusch and 2 more

Open access · greenAbstract read
In one paragraph

Article in Journal of virology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Oral Vaccination with AttenuatedPathogens (Basel, Switzerland) · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. 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

12 authors at 4 institutions in 2 countries.

Ivana KutleInstitute of Virology, Hannover Medical School, Hannover, Germany.
Katarzyna M Szymańska-de WijsInstitute of Virology, Hannover Medical School, Hannover, Germany.
Boris BogdanowProteome Dynamics lab, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Berislav CuvaloInstitute of Virology, Hannover Medical School, Hannover, Germany.
Lars SteinbrückInstitute of Virology, Hannover Medical School, Hannover, Germany.
Stipan JonjićDepartment of Histology and Embryology, Faculty of Medicine, University of Rijeka, Rijeka, Croatia.
Karen WagnerInstitute of Virology, Hannover Medical School, Hannover, Germany.
Rainer NiedenthalInstitute of Cell Biochemistry, Hannover Medical School, Hannover, Germany.
Matthias SelbachProteome Dynamics lab, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Lüder WiebuschLaboratory of Pediatric Molecular Biology, Charité Universitätsmedizin Berlin, Berlin, Germany.
Martina Dezeljin *Institute of Virology, Hannover Medical School, Hannover, Germany.
Martin Messerle *Institute of Virology, Hannover Medical School, Hannover, Germany messerle.martin@mh-hannover.de.ORCID 0000-0002-1227-3933
Medizinische Hochschule Hannover · DEMax Delbrück Center · DECharité - Universitätsmedizin Berlin · DEUniversity of Rijeka · HR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To ensure productive infection, herpesviruses utilize tegument proteins and nonstructural regulatory proteins to counteract cellular defense mechanisms and to reprogram cellular pathways. The M25 proteins of mouse cytomegalovirus (MCMV) belong to the betaherpesvirus UL25 gene family that encodes viral proteins implicated with regulatory functions. Through affinity purification and mass spectrometric analysis, we discovered the tumor suppressor protein p53 as a host factor interacting with the M25 proteins. M25-p53 interaction in infected and transfected cells was confirmed by coimmunoprecipitation. Moreover, the proteins colocalized in nuclear dot-like structures upon both infection and inducible expression of the two M25 isoforms. p53 accumulated in wild-type MCMV-infected cells, while this did not occur upon infection with a mutant lacking the M25 gene. Both M25 proteins were able to mediate the effect, identifying them as the first CMV proteins responsible for p53 accumulation during infection. Interaction with M25 proteins led to substantial prolongation of the half-life of p53. In contrast to the higher abundance of the p53 protein in wild-type MCMV-infected cells, the transcript levels of the prominent p53 target genes

Indexed as

AnimalsCell NucleusHCT116 CellsHEK293 CellsHerpesviridae InfectionsHumansMiceMuromegalovirusTumor Suppressor Protein p53Viral ProteinsTP53 protein, humanTrp53 protein, mouseTumor Suppressor Protein p53Viral ProteinscytomegalovirusM25 proteinsp53virus host cell interaction

Identifiers

PMID32727874
PMCPMC7527045
OpenAlexW3045571324

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.