Evidence map›Paper›PMID 31358914›Full record

ArticleCell death and differentiation2020

JMJD6 modulates DNA damage response through downregulating H4K16ac independently of its enzymatic activity.

Dawei Huo, Hao Chen, Yiming Cheng, Xin Song, Kai Zhang, Mulin Jun Li, Chenghao Xuan

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Mechanism of Histone Arginine Methylation Dynamic Change in Cellular Stress.International journal of molecular sciences · 2024
    Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. 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

7 authors at 1 institution in 1 country.

Dawei HuoTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China.
Hao ChenTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China.
Yiming ChengTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China.
Xin SongTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China.
Kai ZhangTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China.
Mulin Jun LiDepartment of Pharmacology, Tianjin Medical University, 300070, Tianjin, China.ORCID http://orcid.org/0000-0003-3598-3679
Chenghao XuanTianjin Key Laboratory of Medical Epigenetics; Key Laboratory of Breast Cancer Prevention and Therapy (Ministry of Education); Department of Biochemistry and Molecular Biology, Tianjin Medical University, 300070, Tianjin, China. chenghaoxuan@tmu.edu.cn.ORCID http://orcid.org/0000-0002-0179-3781
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The initiation and transduction of DNA damage response (DDR) occur in the context of chromatin, and modifications as well as the structure of chromatin are crucial for DDR signaling. How the profound chromatin alterations are confined to DNA lesions by epigenetic factors remains largely unclear. Here, we discover that JMJD6, a Jumonji C domain-containing protein, is recruited to DNA double-strand breaks (DSBs) after microirradiation. JMJD6 controls the spreading of histone ubiquitination, as well as the subsequent accumulation of repair proteins and transcriptional silencing around DSBs, but does not regulate the initial DNA damage sensing. Furthermore, JMJD6 deficiency results in promotion of the efficiency of nonhomologous end joining (NHEJ) and homologous recombination (HR), rapid cell-cycle checkpoint recovery, and enhanced survival after irradiation. Regarding the mechanism involved, we demonstrate that JMJD6, independently of its catalytic activity, interacts with SIRT1 and recruits it to chromatin to downregulate H4K16ac around DSBs. Our study reveals JMJD6 as a modulator of the epigenome around DNA lesions, and adds to the understanding of the role of epigenetic factors in DNA damage response.

Indexed as

DNA DamageDown-RegulationAcetylationBRCA1 ProteinBromodomain Containing ProteinsCell Cycle ProteinsCell Line, TumorChromatinDNA Breaks, Double-StrandedDNA End-Joining RepairGene SilencingHistonesHomologous RecombinationHumansJumonji Domain-Containing Histone DemethylasesLysineBRCA1 ProteinBRD4 protein, humanBromodomain Containing ProteinsCell Cycle ProteinsChromatinHistonesJMJD6 protein, humanJumonji Domain-Containing Histone DemethylasesLysineSirtuin 1TP53BP1 protein, humanTranscription FactorsTumor Suppressor p53-Binding Protein 1

Identifiers

PMID31358914
PMCPMC7206091
OpenAlexW2965866078

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.