ReviewInternational journal of molecular sciences2023
New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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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.
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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
26 citing papers in PubMed, 35 citations in OpenAlex.
- Fungal DNA damage repair: from model to driver of virulence and AMR.Bioscience reports · 2026Review
- A Comparative Transcriptomic Analysis of X-Ray Irradiation Responses Identifies Candidate Biomarker Genes inInsects · 2026Article
- Transcriptomic analysis of lncRNA-miRNA-mRNA competing endogenous RNA regulatory networks in radiation-induced mouse thymic degeneration.Immunologic research · 2026Article
- Homologous recombination repair germline variants and subsequent neoplasm risk among childhood cancer survivors.JNCI cancer spectrum · 2026Article
- Dose-Dependent Dual Effects of Gradient Ionizing Radiation on Neurocognition.International journal of molecular sciences · 2026Review
- O-GlcNAcylation of NONO mediates alternative splicing of SETMAR and facilitates NHEJ repair.Genome biology · 2026Article
- Chromatin Nano-Organization in Peripheral Blood Mononuclear Cells After In-Solution Irradiation with the Beta-Emitter Lu-177.Biomolecules · 2026Article
- Ionizing radiation: molecular mechanisms, biological effects, and therapeutic targets.Molecular biomedicine · 2026Review
- Article
- Electron Irradiation Effects on N and FeInternational journal of nanomedicine · 2026Article
- BUB1B promotes homologous recombination‑mediated DNA damage repair in breast cancer cells through the PI3K/AKT signaling pathway.Oncology reports · 2025Article
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.Scientific reports · 2025Article
- Molecular and Cellular Effects of CT Scans in Human Adipose Mesenchymal Stem Cells.International journal of molecular sciences · 2025Article
- Assessing the Relative Contribution of DSB Repair Proteins as a Function of LET.International journal of particle therapy · 2025Article
- Trans-Scale Insights into Variability in Radiation Cancer Risk Across Tissues, Individuals, and Species.Biology · 2025Review
- Molecular Mechanisms and Clinical Divergences in HPV-Positive Cervical vs. Oropharyngeal Cancers: A Critical Narrative Review.BMC medicine · 2025Review
- Robotic radiation shielding system reduces radiation-induced DNA damage in operators performing electrophysiological procedures.Scientific reports · 2025Article
- Conversion of Ku80 K568 crotonylation to SUMOylation facilitates DNA non-homologous end joining and cancer radioresistance.Signal transduction and targeted therapy · 2025Article
- Enhanced radiosensitivity of head and neck cancer cells to proton therapy via hyperthermia-induced homologous recombination deficiency.Clinical and translational radiation oncology · 2025Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Radiation therapy is an essential component of present-day cancer management, utilizing ionizing radiation (IR) of different modalities to mitigate cancer progression. IR functions by generating ionizations in cells that induce a plethora of DNA lesions. The most detrimental among them are the DNA double strand breaks (DSBs). In the course of evolution, cells of higher eukaryotes have evolved four major DSB repair pathways: classical non-homologous end joining (c-NHEJ), homologous recombination (HR), alternative end-joining (alt-EJ), and single strand annealing (SSA). These mechanistically distinct repair pathways have different cell cycle- and homology-dependencies but, surprisingly, they operate with widely different fidelity and kinetics and therefore contribute unequally to cell survival and genome maintenance. It is therefore reasonable to anticipate tight regulation and coordination in the engagement of these DSB repair pathway to achieve the maximum possible genomic stability. Here, we provide a state-of-the-art review of the accumulated knowledge on the molecular mechanisms underpinning these repair pathways, with emphasis on c-NHEJ and HR. We discuss factors and processes that have recently come to the fore. We outline mechanisms steering DSB repair pathway choice throughout the cell cycle, and highlight the critical role of DNA end resection in this process. Most importantly, however, we point out the strong preference for HR at low DSB loads, and thus low IR doses, for cells irradiated in the G
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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.