ArticleOpen biology2016
A role for the p53 tumour suppressor in regulating the balance between homologous recombination and non-homologous end joining.
Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 46 citations in OpenAlex.
- Deciphering molecular pathways in urological cancers: A gateway to precision therapeutics.Journal of advanced research · 2026Review
- Specific TP53 mutations impair the recruitment of 53BP1 to DNA double-strand breaks underlying the mechanism of radioresistance.European biophysics journal : EBJ · 2025Article
- Article
- p53-deficient cancer cells hyperactivate DNA double-strand break repair pathways to overcome chemotherapeutic damage and augment survival.Molecular biology reports · 2025Article
- Antitumor Activity of Radiation Therapy Combined with Checkpoint Kinase Inhibition in SHH/International journal of molecular sciences · 2025Article
- Negative feedback loop in the activation of non-homologous end joining DNA repair pathway in Helicobacter pylori infected patients with gastritis.Scientific reports · 2024Article
- DNA methylation profile of inflammatory breast cancer and its impact on prognosis and outcome.Clinical epigenetics · 2024Article
- Utility of Homologous Recombination Deficiency Biomarkers Across Cancer Types.JCO precision oncology · 2022Article
- Article
- Integrated Molecular Analysis Reveals 2 Distinct Subtypes of Pure Seminoma of the Testis.Cancer informatics · 2022Article
- Utility of Homologous Recombination Deficiency Biomarkers Across Cancer Types.JCO precision oncology · 2021Article
- Signaling Pathways in Cancer: Therapeutic Targets, Combinatorial Treatments, and New Developments.Cells · 2021Review
- miR-490 suppresses telomere maintenance program and associated hallmarks in glioblastoma.Cellular and molecular life sciences : CMLS · 2021Article
- Dual inhibition of DNA-PK and DNA polymerase theta overcomes radiation resistance induced by p53 deficiency.NAR cancer · 2020Article
- CHD7 and 53BP1 regulate distinct pathways for the re-ligation of DNA double-strand breaks.Nature communications · 2020Article
- High rate of HDR in gene editing of p.(Thr158Met) MECP2 mutational hotspot.European journal of human genetics : EJHG · 2020Article
- Interaction of Deubiquitinase 2A-DUB/MYSM1 with DNA Repair and Replication Factors.International journal of molecular sciences · 2020Article
- How the Other Half Lives: What p53 Does When It Is Not Being a Transcription Factor.International journal of molecular sciences · 2019Review
- The Chk1 inhibitor SAR-020106 sensitizes human glioblastoma cells to irradiation, to temozolomide, and to decitabine treatment.Journal of experimental & clinical cancer research : CR · 2019Article
- Driver mutations in USP8 wild-type Cushing's disease.Neuro-oncology · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of p53, a transcription factor activated by cellular stress, is a frequent event in cancer. The role of p53 in tumour suppression is largely attributed to cell fate decisions. Here, we provide evidence supporting a novel role for p53 in the regulation of DNA double-strand break (DSB) repair pathway choice. 53BP1, another tumour suppressor, was initially identified as p53 Binding Protein 1, and has been shown to inhibit DNA end resection, thereby stimulating non-homologous end joining (NHEJ). Yet another tumour suppressor, BRCA1, reciprocally promotes end resection and homologous recombination (HR). Here, we show that in both human and mouse cells, the absence of p53 results in impaired 53BP1 focal recruitment to sites of DNA damage induced by ionizing radiation. This effect is largely independent of cell cycle phase and the extent of DNA damage. In p53-deficient cells, diminished localization of 53BP1 is accompanied by a reciprocal increase in BRCA1 recruitment to DSBs. Consistent with these findings, we demonstrate that DSB repair via NHEJ is abrogated, while repair via homology-directed repair (HDR) is stimulated. Overall, we propose that in addition to its role as an 'effector' protein in the DNA damage response, p53 plays a role in the regulation of DSB repair pathway choice.
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Registered trials
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.