Evidence map›Paper›PMID 25698579›Full record

ArticleCell research2015

p53 isoform Δ113p53/Δ133p53 promotes DNA double-strand break repair to protect cell from death and senescence in response to DNA damage.

Lu Gong, Hongjian Gong, Xiao Pan, Changqing Chang, Zhao Ou, Shengfan Ye, Le Yin, Lina Yang, Ting Tao, Zhenhai Zhang and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

76 citing papers in PubMed, 112 citations in OpenAlex.

  1. The p53 Isoforms as Potential Biomarkers in Different Cancer Entities.International journal of molecular sciences · 2026
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  17. Enhancing chimeric antigen receptor T cell therapy by modulating the p53 signaling network with Δ133p53α.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Journal of cardiovascular development and disease · 2023
    Article
  20. Review

16 more citing papers are in PubMed but not listed here.

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

14 authors at 1 institution in 1 country.

Lu GongKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Hongjian GongKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Xiao PanKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Changqing ChangCollege of Natural Resources and Environment, South China Agricultural University, Guangzhou, Guangdong 510650, China.
Zhao OuKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Shengfan YeKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Le YinKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Lina YangKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Ting TaoCollege of Animal Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, Zhenjiang 310058, China.
Zhenhai ZhangNational Key Laboratory of Organ Failure Research, National Clinical Research Center for Kidney Disease, and Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China.
Cong LiuDevelopmental and Stem Cell Institute, West China Second University Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
David P LaneBiomedical Research Council, Agency for Science and Technology Research, Singapore.
Jinrong PengCollege of Animal Sciences, Zhejiang University, 866 Yu Hang Tang Road, Hangzhou, Zhenjiang 310058, China.
Jun ChenKey laboratory for Molecular Animal Nutrition, Ministry of Education, Innovation Center for Signaling Network, College of Life Sciences.
Biomedical Research Council · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The inhibitory role of p53 in DNA double-strand break (DSB) repair seems contradictory to its tumor-suppressing property. The p53 isoform Δ113p53/Δ133p53 is a p53 target gene that antagonizes p53 apoptotic activity. However, information on its functions in DNA damage repair is lacking. Here we report that Δ113p53 expression is strongly induced by γ-irradiation, but not by UV-irradiation or heat shock treatment. Strikingly, Δ113p53 promotes DNA DSB repair pathways, including homologous recombination, non-homologous end joining and single-strand annealing. To study the biological significance of Δ113p53 in promoting DNA DSB repair, we generated a zebrafish Δ113p53(M/M) mutant via the transcription activator-like effector nuclease technique and found that the mutant is more sensitive to γ-irradiation. The human ortholog, Δ133p53, is also only induced by γ-irradiation and functions to promote DNA DSB repair. Δ133p53-knockdown cells were arrested at the G2 phase at the later stage in response to γ-irradiation due to a high level of unrepaired DNA DSBs, which finally led to cell senescence. Furthermore, Δ113p53/Δ133p53 promotes DNA DSB repair via upregulating the transcription of repair genes rad51, lig4 and rad52 by binding to a novel type of p53-responsive element in their promoters. Our results demonstrate that Δ113p53/Δ133p53 is an evolutionally conserved pro-survival factor for DNA damage stress by preventing apoptosis and promoting DNA DSB repair to inhibit cell senescence. Our data also suggest that the induction of Δ133p53 expression in normal cells or tissues provides an important tolerance marker for cancer patients to radiotherapy.

Indexed as

AnimalsAnimals, Genetically ModifiedApoptosisCell LineCellular SenescenceDNADNA-Binding ProteinsDNA Breaks, Double-StrandedDNA Ligase ATPDNA LigasesDNA RepairG2 Phase Cell Cycle CheckpointsHumansPromoter Regions, GeneticProtein BindingProtein IsoformsDNADNA-Binding ProteinsDNA Ligase ATPDNA LigasesLIG4 protein, humanProtein IsoformsRad51 RecombinaseRad52 protein, zebrafishRNA, Small Interferingtp53 protein, zebrafishTumor Suppressor Protein p53Zebrafish Proteins

Identifiers

PMID25698579
PMCPMC4349251
OpenAlexW1964129430

What OpenQuestion holds

Textmetadata
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.