ReviewThe Biochemical journal2009
Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joining.
Review in The Biochemical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 359 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
359 citing papers in PubMed, 695 citations in OpenAlex.
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- Ferroptosis and Radiotherapy in Lung Cancer.Cells · 2025Review
- Activation of Inflammatory and Apoptosis Pathways on Human Gingival Fibroblasts Exposed to Dental Resin Composites.Polymers · 2025Article
- NR4A1 expression aberrations contribute to radiotherapy resistance in gastric cancer.Scientific reports · 2025Article
- Characterizing the structural variations in the genome of the mandarin variety, IrM2, induced by gamma irradiation.Plant biotechnology journal · 2025Article
- Canine Ku70 requires binding between its nuclear localization signal and nuclear pore-targeting complex for nuclear localization.The Journal of veterinary medical science · 2025Article
- Targeting the Werner syndrome protein in microsatellite instability cancers: mechanisms and therapeutic potential.Clinical and experimental medicine · 2025Review
- Manipulating alternative end-joining alters carbon-ion beam-induced genome mutation profiles in Arabidopsis thaliana.DNA research : an international journal for rapid publication of reports on genes and genomes · 2025Article
299 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DNA DSBs (double-strand breaks) are considered the most cytotoxic type of DNA lesion. They can be introduced by external sources such as IR (ionizing radiation), by chemotherapeutic drugs such as topoisomerase poisons and by normal biological processes such as V(D)J recombination. If left unrepaired, DSBs can cause cell death. If misrepaired, DSBs may lead to chromosomal translocations and genomic instability. One of the major pathways for the repair of IR-induced DSBs in mammalian cells is NHEJ (non-homologous end-joining). The main proteins required for NHEJ in mammalian cells are the Ku heterodimer (Ku70/80 heterodimer), DNA-PKcs [the catalytic subunit of DNA-PK (DNA-dependent protein kinase)], Artemis, XRCC4 (X-ray-complementing Chinese hamster gene 4), DNA ligase IV and XLF (XRCC4-like factor; also called Cernunnos). Additional proteins, including DNA polymerases mu and lambda, PNK (polynucleotide kinase) and WRN (Werner's Syndrome helicase), may also play a role. In the present review, we will discuss our current understanding of the mechanism of NHEJ in mammalian cells and discuss the roles of DNA-PKcs and DNA-PK-mediated phosphorylation in NHEJ.
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What OpenQuestion holds
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.