Evidence map›Paper›PMID 22638582›Full record

ArticleNucleic acids research2012

A role for chromatin remodellers in replication of damaged DNA.

Atsuko Niimi, Anna L Chambers, Jessica A Downs, Alan R Lehmann

Abstract read
In one paragraph

Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Histone modification inComputational and structural biotechnology journal · 2023
    Review
  7. Article
  8. Histone sumoylation and chromatin dynamics.Nucleic acids research · 2021
    Review
  9. Article
  10. Article
  11. ACTL6A promotes repair of cisplatin-induced DNA damage, a new mechanism of platinum resistance in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Monoubiquitylation of histone H2B contributes to the bypass of DNA damage during and after DNA replication.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  18. Article
  19. Article
  20. The Many Roles of BAF (mSWI/SNF) and PBAF Complexes in Cancer.Cold Spring Harbor perspectives in medicine · 2016
    Review
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

4 authors.

Atsuko NiimiGenome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK.
Anna L Chambers
Jessica A Downs
Alan R Lehmann

Funding

Cancer Research UK CEA C7905/A10269Medical Research Council G0501450Medical Research Council G1001668
6 · The paper itself

Abstract

In eukaryotic cells, replication past damaged sites in DNA is regulated by the ubiquitination of proliferating cell nuclear antigen (PCNA). Little is known about how this process is affected by chromatin structure. There are two isoforms of the Remodels the Structure of Chromatin (RSC) remodelling complex in yeast. We show that deletion of RSC2 results in a dramatic reduction in the level of PCNA ubiquitination after DNA-damaging treatments, whereas no such effect was observed after deletion of RSC1. Similarly, depletion of the BAF180 component of the corresponding PBAF (Polybromo BRG1 (Brahma-Related Gene 1) Associated Factor) complex in human cells led to a similar reduction in PCNA ubiquitination. Remarkably, we found that depletion of BAF180 resulted after UV-irradiation, in a reduction not only of ubiquitinated PCNA but also of chromatin-associated unmodified PCNA and Rad18 (the E3 ligase that ubiquitinates PCNA). This was accompanied by a modest decrease in fork progression. We propose a model to account for these findings that postulates an involvement of PBAF in repriming of replication downstream from replication forks blocked at sites of DNA damage. In support of this model, chromatin immunoprecipitation data show that the RSC complex in yeast is present in the vicinity of the replication forks, and by extrapolation, this is also likely to be the case for the PBAF complex in human cells.

Indexed as

DNA DamageDNA ReplicationCell CycleCell LineChromatinChromatin Assembly and DisassemblyChromosomal Proteins, Non-HistoneDNA-Binding ProteinsGene DeletionHumansNuclear ProteinsProliferating Cell Nuclear AntigenSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsUbiquitinationChromatinChromosomal Proteins, Non-HistoneDNA-Binding ProteinsINO80 complex, S cerevisiaeNuclear ProteinsPBRM1 protein, humanProliferating Cell Nuclear AntigenRAD18 protein, humanRSC2 protein, S cerevisiaeRSC complex, S cerevisiaeSaccharomyces cerevisiae ProteinsSWI-SNF-B chromatin-remodeling complexTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID22638582
PMCPMC3424576

What OpenQuestion holds

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Registered trials

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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.