ReviewSub-cellular biochemistry2014
Involvement of p53 in the repair of DNA double strand breaks: multifaceted Roles of p53 in homologous recombination repair (HRR) and non-homologous end joining (NHEJ).
Review in Sub-cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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.
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.
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Who cites it
47 citing papers in PubMed, 100 citations in OpenAlex.
- A phase II, randomized, double-blind study of the use of rucaparib vs. placebo maintenance therapy in metastatic and recurrent endometrial cancer.Gynecologic oncology · 2025Trial
- Review
- Multiomic single-cell perturbation screens reveal critical lncRNA regulators of senescence.Nature aging · 2026Article
- Phosphorylation and DNA damage resolution coordinate SOX2-mediated reprogramming in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- POLQ mediated end-joining promotes DNA damage tolerance in neuroblastoma.Translational oncology · 2025Article
- Review
- p53-deficient cancer cells hyperactivate DNA double-strand break repair pathways to overcome chemotherapeutic damage and augment survival.Molecular biology reports · 2025Article
- Gold Nanoparticle-Enhanced Production of Reactive Oxygen Species for Radiotherapy and Phototherapy.Nanomaterials (Basel, Switzerland) · 2025Review
- Decoding the molecular symphony: interactions between the mNAR cancer · 2024Review
- Bromodomain protein BRD4 directs mitotic cell division of mouse fibroblasts by inhibiting DNA damage.iScience · 2024Article
- Mutant p53 reactivation restricts the protumorigenic consequences of wild type p53 loss of heterozygosity in Li-Fraumeni syndrome patient-derived fibroblasts.Cell death and differentiation · 2024Article
- Exploring the Potential of Rosemary Derived Compounds (Rosmarinic and Carnosic Acids) as Cancer Therapeutics: Current Knowledge and Future Perspectives.Biomolecules & therapeutics · 2024Review
- Tumor-specific radiosensitizing effect of the ATM inhibitor AZD0156 in melanoma cells with low toxicity to healthy fibroblasts.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2023Article
- Gene expression of non-homologous end-joining pathways in the prognosis of ovarian cancer.iScience · 2023Article
- The Role of Genetic Polymorphisms in Differentiated Thyroid Cancer: A 2023 Update.Biomedicines · 2023Review
- Relative biological effectiveness of low-energy X-rays (25 kV) in mutant p53 cancer cells.Radiation and environmental biophysics · 2023Article
- Inactivation of RB1, CDKN2A, and TP53 have distinct effects on genomic stability at side-by-side comparison in karyotypically normal cells.Genes, chromosomes & cancer · 2023Article
- Physapruin A Enhances DNA Damage and Inhibits DNA Repair to Suppress Oral Cancer Cell Proliferation.International journal of molecular sciences · 2022Article
- A pan-cancer compendium of chromosomal instability.Nature · 2022Article
- Rapid recruitment of p53 to DNA damage sites directs DNA repair choice and integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
p53 is a tumor suppressor protein that prevents oncogenic transformation and maintains genomic stability by blocking proliferation of cells harboring unrepaired or misrepaired DNA. A wide range of genotoxic stresses such as DNA damaging anti-cancer drugs and ionizing radiation promote nuclear accumulation of p53 and trigger its ability to activate or repress a number of downstream target genes involved in various signaling pathways. This cascade leads to the activation of multiple cell cycle checkpoints and subsequent cell cycle arrest, allowing the cells to either repair the DNA or undergo apoptosis, depending on the intensity of DNA damage. In addition, p53 has many transcription-independent functions, including modulatory roles in DNA repair and recombination. This chapter will focus on the role of p53 in regulating or influencing the repair of DNA double-strand breaks that mainly includes homologous recombination repair (HRR) and non-homologous end joining (NHEJ). Through this discussion, we will try to establish that p53 acts as an important linchpin between upstream DNA damage signaling cues and downstream cellular events that include repair, recombination, and apoptosis.
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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.