Evidence map›Paper›PMID 29955842›Full record

ArticleNucleic acids research2018

The transcription-coupled DNA repair-initiating protein CSB promotes XRCC1 recruitment to oxidative DNA damage.

Hervé Menoni, Franziska Wienholz, Arjan F Theil, Roel C Janssens, Hannes Lans, Anna Campalans, J Pablo Radicella, Jurgen A Marteijn, Wim Vermeulen

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 70 citations in OpenAlex.

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  13. Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022
    Review
  14. Article
  15. Article
  16. XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022
    Review
  17. Article
  18. Article
  19. Article
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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

9 authors at 3 institutions in 2 countries.

Hervé MenoniDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Franziska WienholzDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Arjan F TheilDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Roel C JanssensDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Hannes LansDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Anna CampalansCEA, Institute of Cellular and Molecular Radiobiology, F-96265 Fontenay aux Roses, France.
J Pablo RadicellaCEA, Institute of Cellular and Molecular Radiobiology, F-96265 Fontenay aux Roses, France.
Jurgen A MarteijnDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Wim VermeulenDepartment of Molecular Genetics, Oncode Institute, Cancer Genomics Netherlands, Erasmus MC, Dr. Molewaterplein 40, 3015 GD Rotterdam, The Netherlands.
Erasmus MC · NLInserm · FRUniversité Claude Bernard Lyon 1 · FR

Funding

European Research Council 340988
6 · The paper itself

Abstract

Transcription-coupled nucleotide excision repair factor Cockayne syndrome protein B (CSB) was suggested to function in the repair of oxidative DNA damage. However thus far, no clear role for CSB in base excision repair (BER), the dedicated pathway to remove abundant oxidative DNA damage, could be established. Using live cell imaging with a laser-assisted procedure to locally induce 8-oxo-7,8-dihydroguanine (8-oxoG) lesions, we previously showed that CSB is recruited to these lesions in a transcription-dependent but NER-independent fashion. Here we showed that recruitment of the preferred 8-oxoG-glycosylase 1 (OGG1) is independent of CSB or active transcription. In contrast, recruitment of the BER-scaffolding protein, X-ray repair cross-complementing protein 1 (XRCC1), to 8-oxoG lesions is stimulated by CSB and transcription. Remarkably, recruitment of XRCC1 to BER-unrelated single strand breaks (SSBs) does not require CSB or transcription. Together, our results suggest a specific transcription-dependent role for CSB in recruiting XRCC1 to BER-generated SSBs, whereas XRCC1 recruitment to SSBs generated independently of BER relies predominantly on PARP activation. Based on our results, we propose a model in which CSB plays a role in facilitating BER progression at transcribed genes, probably to allow XRCC1 recruitment to BER-intermediates masked by RNA polymerase II complexes stalled at these intermediates.

Indexed as

DNA DamageDNA RepairTranscription, GeneticCell LineDNADNA HelicasesDNA Repair EnzymesHEK293 CellsHumansModels, GeneticOxidation-ReductionOxidative StressPoly-ADP-Ribose Binding ProteinsX-ray Repair Cross Complementing Protein 1DNADNA HelicasesDNA Repair EnzymesERCC6 protein, humanPoly-ADP-Ribose Binding ProteinsX-ray Repair Cross Complementing Protein 1XRCC1 protein, human

Identifiers

PMID29955842
PMCPMC6125634
OpenAlexW2811024396

What OpenQuestion holds

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LicenceCC BY-NC
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.