Evidence map›Paper›PMID 19797077›Full record

ArticleThe Journal of cell biology2009

Nucleotide excision repair-induced H2A ubiquitination is dependent on MDC1 and RNF8 and reveals a universal DNA damage response.

Jurgen A Marteijn, Simon Bekker-Jensen, Niels Mailand, Hannes Lans, Petra Schwertman, Audrey M Gourdin, Nico P Dantuma, Jiri Lukas, Wim Vermeulen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
108citing papers in PubMed, 1 pooled it
8.9field-weighted citation impact, top 1% 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

108 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Epigenetic Regulation of Nucleotide Excision Repair.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. Article

48 more citing papers are in PubMed but not listed here.

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 3 countries.

Jurgen A MarteijnDepartment of Genetics, Center for Biomedical Genetics, Erasmus Medical Center, 3015 GE Rotterdam, Netherlands.
Simon Bekker-Jensen
Niels Mailand
Hannes Lans
Petra Schwertman
Audrey M Gourdin
Nico P Dantuma
Jiri Lukas
Wim Vermeulen
Erasmus MC · NLDanish Cancer Society · DKKarolinska Institutet · SE

Funding

Worldwide Cancer Research 08-0084
6 · The paper itself

Abstract

Chromatin modifications are an important component of the of DNA damage response (DDR) network that safeguard genomic integrity. Recently, we demonstrated nucleotide excision repair (NER)-dependent histone H2A ubiquitination at sites of ultraviolet (UV)-induced DNA damage. In this study, we show a sustained H2A ubiquitination at damaged DNA, which requires dynamic ubiquitination by Ubc13 and RNF8. Depletion of these enzymes causes UV hypersensitivity without affecting NER, which is indicative of a function for Ubc13 and RNF8 in the downstream UV-DDR. RNF8 is targeted to damaged DNA through an interaction with the double-strand break (DSB)-DDR scaffold protein MDC1, establishing a novel function for MDC1. RNF8 is recruited to sites of UV damage in a cell cycle-independent fashion that requires NER-generated, single-stranded repair intermediates and ataxia telangiectasia-mutated and Rad3-related protein. Our results reveal a conserved pathway of DNA damage-induced H2A ubiquitination for both DSBs and UV lesions, including the recruitment of 53BP1 and Brca1. Although both lesions are processed by independent repair pathways and trigger signaling responses by distinct kinases, they eventually generate the same epigenetic mark, possibly functioning in DNA damage signal amplification.

Indexed as

DNA DamageDNA RepairProtein Processing, Post-TranslationalUltraviolet RaysAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCell Cycle ProteinsDNADNA-Binding ProteinsDose-Response Relationship, RadiationEpigenesis, GeneticHeLa CellsHistonesHumansIntracellular Signaling Peptides and ProteinsAdaptor Proteins, Signal TransducingAtaxia Telangiectasia Mutated ProteinsATR protein, humanBRCA1 ProteinBRCA1 protein, humanCell Cycle ProteinsDNADNA-Binding ProteinsHistonesIntracellular Signaling Peptides and ProteinsMDC1 protein, humanNuclear ProteinsProtein Serine-Threonine KinasesRecombinant Fusion ProteinsRNF8 protein, humanTP53BP1 protein, humanTrans-ActivatorsTumor Suppressor p53-Binding Protein 1UBE2N protein, humanUbiquitin-Conjugating EnzymesUbiquitin-Protein LigasesXPC protein, human

Identifiers

PMID19797077
PMCPMC2753161
OpenAlexW2032739040

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.