Evidence map›Paper›PMID 32908893›Full record

ReviewBioMed research international2020

The Determinant of DNA Repair Pathway Choices in Ionising Radiation-Induced DNA Double-Strand Breaks.

Lei Zhao, Chengyu Bao, Yuxuan Shang, Xinye He, Chiyuan Ma, Xiaohua Lei, Dong Mi, Yeqing Sun

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

32 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
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  3. APOL2 Stabilizes Ku80 to Confer NHEJ-Mediated Radioresistance in Gastric Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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  16. Roles of NRF2 in DNA damage repair.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  17. Review
  18. Review
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  20. 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

8 authors at 2 institutions in 1 country.

Lei ZhaoInstitute of Environmental Systems Biology, College of Environmental Science and Engineering, Dalian Maritime University, Dalian, 116026 Liaoning, China.ORCID https://orcid.org/0000-0001-5912-2676
Chengyu BaoInstitute of Environmental Systems Biology, College of Environmental Science and Engineering, Dalian Maritime University, Dalian, 116026 Liaoning, China.
Yuxuan ShangInstitute of Environmental Systems Biology, College of Environmental Science and Engineering, Dalian Maritime University, Dalian, 116026 Liaoning, China.
Xinye HeInstitute of Environmental Systems Biology, College of Environmental Science and Engineering, Dalian Maritime University, Dalian, 116026 Liaoning, China.
Chiyuan MaState Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Xiaohua LeiState Key Laboratory of Stem Cell and Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.ORCID https://orcid.org/0000-0001-8095-9008
Dong MiCollege of Science, Dalian Maritime University, Dalian, Liaoning, China.
Yeqing SunInstitute of Environmental Systems Biology, College of Environmental Science and Engineering, Dalian Maritime University, Dalian, 116026 Liaoning, China.ORCID https://orcid.org/0000-0002-8708-9962
Dalian Maritime University · CNChinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionising radiation- (IR-) induced DNA double-strand breaks (DSBs) are considered to be the deleterious DNA lesions that pose a serious threat to genomic stability. The major DNA repair pathways, including classical nonhomologous end joining, homologous recombination, single-strand annealing, and alternative end joining, play critical roles in countering and eliciting IR-induced DSBs to ensure genome integrity. If the IR-induced DNA DSBs are not repaired correctly, the residual or incorrectly repaired DSBs can result in genomic instability that is associated with certain human diseases. Although many efforts have been made in investigating the major mechanisms of IR-induced DNA DSB repair, it is still unclear what determines the choices of IR-induced DNA DSB repair pathways. In this review, we discuss how the mechanisms of IR-induced DSB repair pathway choices can operate in irradiated cells. We first briefly describe the main mechanisms of the major DNA DSB repair pathways and the related key repair proteins. Based on our understanding of the characteristics of IR-induced DNA DSBs and the regulatory mechanisms of DSB repair pathways in irradiated cells and recent advances in this field, We then highlight the main factors and associated challenges to determine the IR-induced DSB repair pathway choices. We conclude that the type and distribution of IR-induced DSBs, chromatin state, DNA-end structure, and DNA-end resection are the main determinants of the choice of the IR-induced DNA DSB repair pathway.

Indexed as

Radiation, IonizingAnimalsCell CycleChromatinDNADNA Breaks, Double-StrandedDNA RepairGenomic InstabilityHomologous RecombinationHumansChromatinDNA

Identifiers

PMID32908893
PMCPMC7468606
OpenAlexW3080968360

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.