Evidence map›Paper›PMID 38936834›Full record

ArticleNucleic acids research2024

PCAF promotes R-loop resolution via histone acetylation.

Seo Yun Lee, Soo Hyeon Lee, Nak Hun Choi, Ja Young Kim, Jun Hee Kweon, Kyle M Miller, Jae Jin Kim

Abstract read
In one paragraph

Article in Nucleic acids research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. R-loops: a key driver of inflammatory responses in cancer.Experimental & molecular medicine · 2025
    Review
  15. Wdr5-mediated H3K4 methylation facilitates HSPC development via maintenance of genomic stability in zebrafish.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  16. Article
  17. Review
  18. 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.

Seo Yun LeeDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.ORCID 0000-0003-2552-9990
Soo Hyeon LeeDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.
Nak Hun ChoiDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.
Ja Young KimDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.
Jun Hee KweonDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.
Kyle M MillerDepartment of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA.ORCID 0000-0002-4544-0013
Jae Jin KimDepartment of Life Science and Multidisciplinary Genome Institute, Hallym University, Chuncheon 24252, Republic of Korea.ORCID 0009-0005-6645-8094

Funding

Shaping DNA Damage Response Networks Via Histone H2A VariantsR01CA198279 · NCI · UNIVERSITY OF TEXAS AT AUSTIN · PI Kyle M Miller · 2016 to 2026
$3.3M
Mechanisms of Endogenous DNA Damage PromotionR01CA250905 · NCI · BAYLOR COLLEGE OF MEDICINE · PI MILLER, KYLE M, ROSENBERG, SUSAN M · 2020 to 2024
$3.3M
Korea government (MIST) NRF- 2022R1C1C1007759National Research Foundation of KoreaNCI NIH HHS R01 CA198279NCI NIH HHS R01 CA250905NCI NIH HHS RO1 CA198279
6 · The paper itself

Abstract

R-loops cause genome instability, disrupting normal cellular functions. Histone acetylation, particularly by p300/CBP-associated factor (PCAF), is essential for maintaining genome stability and regulating cellular processes. Understanding how R-loop formation and resolution are regulated is important because dysregulation of these processes can lead to multiple diseases, including cancer. This study explores the role of PCAF in maintaining genome stability, specifically for R-loop resolution. We found that PCAF depletion promotes the generation of R-loop structures, especially during ongoing transcription, thereby compromising genome stability. Mechanistically, we found that PCAF facilitates histone H4K8 acetylation, leading to recruitment of the a double-strand break repair protein (MRE11) and exonuclease 1 (EXO1) to R-loop sites. These in turn recruit Fanconi anemia (FA) proteins, including FANCM and BLM, to resolve the R-loop structure. Our findings suggest that PCAF, histone acetylation, and FA proteins collaborate to resolve R-loops and ensure genome stability. This study therefore provides novel mechanistic insights into the dynamics of R-loops as well as the role of PCAF in preserving genome stability. These results may help develop therapeutic strategies to target diseases associated with genome instability.

Indexed as

Genomic InstabilityHistonesp300-CBP Transcription FactorsR-Loop StructuresAcetylationDNA RepairDNA Repair EnzymesExodeoxyribonucleasesHumansp300-CBP-Associated FactorDNA Repair EnzymesEXO1 protein, humanExodeoxyribonucleasesHistonesp300-CBP-Associated Factorp300-CBP Transcription Factors

Identifiers

PMID38936834
PMCPMC11347145

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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.