Evidence map›Paper›PMID 28740167›Full record

ArticleNature communications2017

DNA end resection requires constitutive sumoylation of CtIP by CBX4.

Isabel Soria-Bretones, Cristina Cepeda-García, Cintia Checa-Rodriguez, Vincent Heyer, Bernardo Reina-San-Martin, Evi Soutoglou, Pablo Huertas

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. SUMO and the DNA damage response.Biochemical Society transactions · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Advances in SUMO-based regulation of homologous recombination.Current opinion in genetics & development · 2021
    Review
  17. Review
  18. ATM controls the extent of DNA end resection by eliciting sequential posttranslational modifications of CtIP.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  19. Article
  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

7 authors at 2 institutions in 2 countries.

Isabel Soria-BretonesDepartamento de Genética, Universidad de Sevilla, Sevilla, 41080, Spain.
Cristina Cepeda-GarcíaCentro Andaluz de Biología Molecular y Medicina Regenerativa-CABIMER, Universidad de Sevilla-CSIC-Universidad Pablo de Olavide, Sevilla, 41092, Spain.
Cintia Checa-RodriguezDepartamento de Genética, Universidad de Sevilla, Sevilla, 41080, Spain.
Vincent HeyerInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, 67404, France.
Bernardo Reina-San-MartinInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, 67404, France.
Evi SoutoglouInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, 67404, France.
Pablo HuertasDepartamento de Genética, Universidad de Sevilla, Sevilla, 41080, Spain. pablo.huertas@cabimer.es.ORCID http://orcid.org/0000-0002-1756-4449
Centro Andaluz de Biología Molecular y Medicina Regenerativa · ESInstitut de génétique et de biologie moléculaire et cellulaire · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA breaks are complex DNA lesions that can be repaired by two alternative mechanisms: non-homologous end-joining and homologous recombination. The decision between them depends on the activation of the DNA resection machinery, which blocks non-homologous end-joining and stimulates recombination. On the other hand, post-translational modifications play a critical role in DNA repair. We have found that the SUMO E3 ligase CBX4 controls resection through the key factor CtIP. Indeed, CBX4 depletion impairs CtIP constitutive sumoylation and DNA end processing. Importantly, mutating lysine 896 in CtIP recapitulates the CBX4-depletion phenotype, blocks homologous recombination and increases genomic instability. Artificial fusion of CtIP and SUMO suppresses the effects of both the non-sumoylatable CtIP mutant and CBX4 depletion. Mechanistically, CtIP sumoylation is essential for its recruitment to damaged DNA. In summary, sumoylation of CtIP at lysine 896 defines a subpopulation of the protein that is involved in DNA resection and recombination.The choice between non-homologous end-joining and homologous recombination to repair a DNA double-strand break depends on activation of the end resection machinery. Here the authors show that SUMO E3 ligase CBX4 sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.

Indexed as

DNA Breaks, Double-StrandedDNA End-Joining RepairBlotting, WesternCarrier ProteinsCell Line, TumorDNAEndodeoxyribonucleasesHEK293 CellsHomologous RecombinationHumansLigasesMicroscopy, ConfocalNuclear ProteinsPolycomb-Group ProteinsRNA InterferenceSmall Ubiquitin-Related Modifier ProteinsCarrier ProteinsCBX4 protein, humanDNAEndodeoxyribonucleasesLigasesNuclear ProteinsPolycomb-Group ProteinsRBBP8 protein, humanSmall Ubiquitin-Related Modifier ProteinsSUMO-1 ProteinSUMO1 protein, humanSUMO2 protein, human

Identifiers

PMID28740167
PMCPMC5524638
OpenAlexW2735621267

What OpenQuestion 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 OpenQuestion graph.