ArticleOncogene2001
Efficient rejoining of radiation-induced DNA double-strand breaks in vertebrate cells deficient in genes of the RAD52 epistasis group.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 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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Who cites it
54 citing papers in PubMed, 172 citations in OpenAlex.
- New Facets of DNA Double Strand Break Repair: Radiation Dose as Key Determinant of HR versus c-NHEJ Engagement.International journal of molecular sciences · 2023Review
- Article
- Kinome-wide screening uncovers a role for Bromodomain Protein 3 in DNA double-stranded break repair.DNA repair · 2023Article
- Increased Gene Targeting in Hyper-Recombinogenic LymphoBlastoid Cell Lines Leaves Unchanged DSB Processing by Homologous Recombination.International journal of molecular sciences · 2022Article
- Alternative end-joining in BCR gene rearrangements and translocations.Acta biochimica et biophysica Sinica · 2022Review
- The Chromatin Architectural Protein CTCF Is Critical for Cell Survival upon Irradiation-Induced DNA Damage.International journal of molecular sciences · 2022Article
- Impaired DNA Repair Fidelity in a Breast Cancer Patient With Adverse Reactions to Radiotherapy.Frontiers in public health · 2021Article
- Strong suppression of gene conversion with increasing DNA double-strand break load delimited by 53BP1 and RAD52.Nucleic acids research · 2020Article
- Predicting DNA damage foci and their experimental readout with 2D microscopy: a unified approach applied to photon and neutron exposures.Scientific reports · 2019Article
- Single-dose radiotherapy disables tumor cell homologous recombination via ischemia/reperfusion injury.The Journal of clinical investigation · 2019Article
- PARP1 is required for preserving telomeric integrity but is dispensable for A-NHEJ.Oncotarget · 2018Article
- Investigation of dose-rate effects and cell-cycle distribution under protracted exposure to ionizing radiation for various dose-rates.Scientific reports · 2018Article
- Pold3 is required for genomic stability and telomere integrity in embryonic stem cells and meiosis.Nucleic acids research · 2018Article
- AUNIP/C1orf135 directs DNA double-strand breaks towards the homologous recombination repair pathway.Nature communications · 2017Article
- Deregulated BCL-2 family proteins impact on repair of DNA double-strand breaks and are targets to overcome radioresistance in lung cancer.Journal of cancer research and clinical oncology · 2017Article
- Biological determinants of radioresistance and their remediation in pancreatic cancer.Biochimica et biophysica acta. Reviews on cancer · 2017Review
- Biology of high single doses of IORT: RBE, 5 R's, and other biological aspects.Radiation oncology (London, England) · 2017Review
- Mechanistic Modelling and Bayesian Inference Elucidates the Variable Dynamics of Double-Strand Break Repair.PLoS computational biology · 2016Article
- Cancer risk at low doses of ionizing radiation: artificial neural networks inference from atomic bomb survivors.Journal of radiation research · 2014Review
- DNA ligases I and III cooperate in alternative non-homologous end-joining in vertebrates.PloS one · 2013Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Rejoining of ionizing radiation (IR) induced DNA DSBs usually follows biphasic kinetics with a fast (t(50): 5-30 min) component attributed to DNA-PK-dependent non-homologous endjoining (NHEJ) and a slow (t(50): 1-20 h), as of yet uncharacterized, component. To examine whether homologous recombination (HR) contributes to DNA DSB rejoining, a systematic genetic study was undertaken using the hyper-recombinogenic DT40 chicken cell line and a series of mutants defective in HR. We show that DT40 cells rejoin IR-induced DNA DSBs with half times of 13 min and 4.5 h and contributions by the fast (78%) and the slow (22%) components similar to those of other vertebrate cells with 1000-fold lower levels of HR. We also show that deletion of RAD51B, RAD52 and RAD54 leaves unchanged the rejoining half times and the contribution of the slow component, as does also a conditional knock out mutant of RAD51. A significant reduction (to 37%) in the contribution of the fast component is observed in Ku70(-/-) DT40 cells, but the slow component, operating with a half time of 18.4 h, is still able to rejoin the majority (63%) of DSBs. A double mutant Ku70(-/-)/RAD54(-/-) shows similar half times to Ku70(-/-) cells. Thus, variations in HR by several orders of magnitude leave unchanged the kinetics of rejoining of DNA DSBs, and fail to modify the contribution of the slow component in a way compatible with a dependence on HR. We propose that, in contrast to yeast, cells of vertebrates are 'hard-wired' in the utilization of NHEJ as the main pathway for rejoining of IR-induced DNA DSBs and speculate that the contribution of homologous recombination repair (HRR) is at a stage after the initial rejoining.
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