Evidence map›Paper›PMID 24413084›Full record

ArticleOncogene2015

ATM-mediated phosphorylation of the chromatin remodeling enzyme BRG1 modulates DNA double-strand break repair.

S-J Kwon, J-H Park, E-J Park, S-A Lee, H-S Lee, S W Kang, J Kwon

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Review
  3. The role of SMARCA4 in lung cancer.Scientific reports · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. On the Interaction Between SMARCAL1 and BRG1.Frontiers in cell and developmental biology · 2022
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Zinc finger protein E4F1 cooperates with PARP-1 and BRG1 to promote DNA double-strand break repair.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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 1 institution in 1 country.

S-J KwonDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
J-H ParkDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
E-J ParkDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
S-A LeeDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
H-S LeeDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
S W KangDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
J KwonDepartment of Life Science, College of Natural Sciences, The Research Center for Cellular Homeostasis, Ewha Womans University, Seoul, Republic of Korea.
Ewha Womans University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP-dependent chromatin remodeling complexes such as SWI/SNF (SWItch/Sucrose NonFermentable) have been implicated in DNA double-strand break (DSB) repair and damage responses. However, the regulatory mechanisms that control the function of chromatin remodelers in DNA damage response are largely unknown. Here, we show that ataxia telangiectasia mutated (ATM) mediates the phosphorylation of BRG1, the catalytic ATPase of the SWI/SNF complex that contributes to DSB repair by binding γ-H2AX-containing nucleosomes via interaction with acetylated histone H3 and stimulating γ-H2AX formation, at Ser-721 in response to DNA damage. ATM-mediated phosphorylation of BRG1 occurs rapidly and transiently after DNA damage. Phosphorylated BRG1 binds γ-H2AX-containing nucleosomes to form the repair foci. The Ser-721 phosphorylation of BRG1 is critical for binding γ-H2AX-containing nucleosomes and stimulating γ-H2AX formation and DSB repair. BRG1 binds to acetylated H3 peptides much better after phosphorylation at Ser-721 by DNA damage. However, the phosphorylation of Ser-721 does not significantly affect the ATPase and transcriptional activities of BRG1. These results, establishing BRG1 as a novel and functional ATM substrate, suggest that the ATM-mediated phosphorylation of BRG1 facilitates DSB repair by stimulating the association of this remodeler with γ-H2AX nucleosomes via enhancing the affinity to acetylated H3. Our work also suggests that the mechanism of BRG1 stimulation of DNA repair is independent of the remodeler's enzymatic or transcriptional activities.

Indexed as

DNA RepairAcetylationAtaxia Telangiectasia Mutated ProteinsCell Line, TumorChromatin Assembly and DisassemblyDNA Breaks, Double-StrandedDNA HelicasesHEK293 CellsHeLa CellsHistonesHumansImmunoblottingMicroscopy, ConfocalMutationNuclear ProteinsNucleosomesAtaxia Telangiectasia Mutated ProteinsDNA HelicasesH2AX protein, humanHistonesNuclear ProteinsNucleosomesSerineSMARCA4 protein, humanTranscription Factors

Identifiers

PMID24413084
OpenAlexW2083022228

What OpenQuestion holds

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Read underepoch 390

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.