Evidence map›Paper›PMID 33101843›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020

ATM-Dependent Recruitment of BRD7 is required for Transcriptional Repression and DNA Repair at DNA Breaks Flanking Transcriptional Active Regions.

Kaishun Hu, Yu Li, Wenjing Wu, Limin Xie, Haiyan Yan, Yuexin Cai, Dong Chen, Qiongchao Jiang, Lehang Lin, Zhen Chen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Nucleoporins cooperate with Polycomb silencers to promote transcriptional repression and repair at DNA double-strand breaks.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Review
  5. Review
  6. The Role of SWI/SNF Complex in Bladder Cancer.Journal of cellular and molecular medicine · 2025
    Review
  7. Article
  8. Article
  9. Calmodulin Triggers Activity-Dependent rRNA Biogenesis via Interaction with DDX21.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. 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

15 authors at 2 institutions in 2 countries.

Kaishun HuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Yu LiGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Wenjing WuGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Limin XieGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Haiyan YanGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Yuexin CaiGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Dong ChenGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Qiongchao JiangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Lehang LinGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Zhen ChenGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Jian-You LiaoGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Yin ZhangGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
H Phillip KoefflerDivision of Hematology/Oncology Cedars-Sinai Medical Center University of California Los Angeles School of Medicine Los Angeles CA 90048 USA.
Dong YinGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.ORCID https://orcid.org/0000-0003-1494-7185
Erwei SongGuangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation Medical Research Center Sun Yat-Sen Memorial Hospital Sun Yat-Sen University Guangzhou 510120 China.
Sun Yat-sen University · CNCedars-Sinai Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Repair of DNA double-strand breaks (DSBs) is essential for genome integrity, and is accompanied by transcriptional repression at the DSB regions. However, the mechanisms how DNA repair induces transcriptional inhibition remain elusive. Here, it is identified that BRD7 participates in DNA damage response (DDR) and is recruited to the damaged chromatin via ATM signaling. Mechanistically, BRD7 joins the polycomb repressive complex 2 (PRC2), the nucleosome remodeling and histone deacetylation (NuRD) complex at the damaged DNA and recruits E3 ubiquitin ligase RNF168 to the DSBs. Furthermore, ATM-mediated BRD7 phosphorylation is required for recruitment of the PRC2 complex, NuRD complex, DSB sensor complex MRE11-RAD50-NBS1 (MRN), and RNF168 to the active transcription sites at DSBs, resulting in transcriptional repression and DNA repair. Moreover, BRD7 deficiency sensitizes cancer cells to PARP inhibition. Collectively, BRD7 is crucial for DNA repair and DDR-mediated transcription repression, which may serve as a therapeutic target. The findings identify the missing link between DNA repair and transcription regulation that maintains genome integrity.

Indexed as

ATMBRD7NuRDPRC2transcriptional repression

Identifiers

PMID33101843
PMCPMC7578904
OpenAlexW3082211052

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.