Evidence map›Paper›PMID 26876210›Full record

ArticleOncogene2016

Rad54 and Mus81 cooperation promotes DNA damage repair and restrains chromosome missegregation.

S El Ghamrasni, R Cardoso, L Li, K K N Guturi, V A Bjerregaard, Y Liu, S Venkatesan, M P Hande, J T Henderson, O Sanchez and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Germline Mutation inCancers · 2020
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. 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

13 authors at 6 institutions in 3 countries.

S El GhamrasniDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
R CardosoDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
L LiDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
K K N GuturiDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
V A BjerregaardDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Ageing, University of Copenhagen, Panum Institute, Copenhagen, Denmark.
Y LiuDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Ageing, University of Copenhagen, Panum Institute, Copenhagen, Denmark.
S VenkatesanDepartment of Physiology, Yong Loo Lin School of Medicine and Tembusu College, National University of Singapore, Singapore.
M P HandeDepartment of Physiology, Yong Loo Lin School of Medicine and Tembusu College, National University of Singapore, Singapore.
J T HendersonDepartment of Pharmaceutical Sciences, Division of Biomolecular Science, Leslie Dan Faculty of Pharmacy, University of Toronto, Toronto, Ontario, Canada.
O SanchezDepartment of pathology, University of Ontario Institute of Technology, Oshawa, Ontario, Canada.
I D HicksonDepartment of Cellular and Molecular Medicine, Center for Chromosome Stability and Center for Healthy Ageing, University of Copenhagen, Panum Institute, Copenhagen, Denmark.
A HakemDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
R HakemDepartment of Medical Biophysics, University of Toronto and Princess Margaret Cancer Centre, University Health Network, Toronto, Ontario, Canada.
University of Copenhagen · DKUniversity of Toronto · CANational University of Singapore · SGPrincess Margaret Cancer Centre · CAUniversity Health Network · CAUniversity of Ontario Institute of Technology · CA

Funding

CIHR
6 · The paper itself

Abstract

Rad54 and Mus81 mammalian proteins physically interact and are important for the homologous recombination DNA repair pathway; however, their functional interactions in vivo are poorly defined. Here, we show that combinatorial loss of Rad54 and Mus81 results in hypersensitivity to DNA-damaging agents, defects on both the homologous recombination and non-homologous DNA end joining repair pathways and reduced fertility. We also observed that while Mus81 deficiency diminished the cleavage of common fragile sites, very strikingly, Rad54 loss impaired this cleavage to even a greater extent. The inefficient repair of DNA double-strand breaks (DSBs) in Rad54(-/-)Mus81(-/-) cells was accompanied by elevated levels of chromosome missegregation and cell death. Perhaps as a consequence, tumor incidence in Rad54(-/-)Mus81(-/-) mice remained comparable to that in Mus81(-/-) mice. Our study highlights the importance of the cooperation between Rad54 and Mus81 for mediating DNA DSB repair and restraining chromosome missegregation.

Indexed as

AnimalsChromosomesDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA DamageDNA End-Joining RepairDNA HelicasesDNA RepairEndonucleasesHomologous RecombinationHumansMiceMice, KnockoutNeoplasmsNuclear ProteinsDNA-Binding ProteinsDNA HelicasesEndonucleasesMus81 protein, mouseNuclear ProteinsRad54l protein, mouse

Identifiers

PMID26876210
OpenAlexW2278698827

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.