ArticleISRN molecular biology2012
Processing of damaged DNA ends for double-strand break repair in mammalian cells.
Article in ISRN molecular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 76 citations in OpenAlex.
- Core NHEJ Factors Maintain Synapsis Across Diverse DNA End Structures.bioRxiv : the preprint server for biology · 2026Article
- DNA polymerase λ autoinhibition is relieved via Ku interaction during non-homologous end joining.Nucleic acids research · 2026Article
- Dirty Ends: Formation, Repair, and Biological Relevance of Non-Canonical DNA Terminal Structures.Genes · 2025Review
- Hydrogen peroxide sulfenylates and inhibits the photorespiratory enzyme PGLP1 to modulate plant thermotolerance.Plant communications · 2024Article
- Targeting the DNA Damage Response for Cancer Therapy.International journal of molecular sciences · 2023Review
- Article
- Transmembrane nuclease NUMEN/ENDOD1 regulates DNA repair pathway choice at the nuclear periphery.Nature cell biology · 2023Article
- HPV integration generates a cellular super-enhancer which functions as ecDNA to regulate genome-wide transcription.Nucleic acids research · 2023Article
- Article
- A Mechanism to Minimize Errors during Non-homologous End Joining.Molecular cell · 2020Article
- CNCC: an analysis tool to determine genome-wide DNA break end structure at single-nucleotide resolution.BMC genomics · 2020Article
- Tyrosyl-DNA Phosphodiesterase I N-Terminal Domain Modifications and Interactions Regulate Cellular Function.Genes · 2019Review
- Clustered DNA Damages induced by 0.5 to 30 eV Electrons.International journal of molecular sciences · 2019Review
- "An End to a Means": How DNA-End Structure Shapes the Double-Strand Break Repair Process.Frontiers in molecular biosciences · 2019Review
- Evolutionary diversity and novelty of DNA repair genes in asexual Bdelloid rotifers.BMC evolutionary biology · 2018Article
- TDP1 suppresses mis-joining of radiomimetic DNA double-strand breaks and cooperates with Artemis to promote optimal nonhomologous end joining.Nucleic acids research · 2018Article
- Nonhomologous DNA end-joining for repair of DNA double-strand breaks.The Journal of biological chemistry · 2018Review
- The Interaction of the Metallo-Glycopeptide Anti-Tumour Drug Bleomycin with DNA.International journal of molecular sciences · 2018Review
- Tyrosyl-DNA phosphodiesterases: rescuing the genome from the risks of relaxation.Nucleic acids research · 2018Review
- Ape1 guides DNA repair pathway choice that is associated with drug tolerance in glioblastoma.Scientific reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Most DNA double-strand breaks (DSBs)formed in a natural environment have chemical modifications at or near the ends that preclude direct religation and require removal or other processing so that rejoining can proceed. Free radical-mediated DSBs typically bear unligatable 3'-phosphate or 3'-phosphoglycolate termini and often have oxidized bases and/or abasic sites near the break. Topoisomerase-mediated DSBs are blocked by covalently bound peptide fragments of the topoisomerase. Enzymes capable of resolving damaged ends include polynucleotide kinase/phosphatase, which restores missing 5'-phosphates and removes 3'-phosphates; tyrosyl-DNA phosphodiesterases I and II (TDP1 and TDP2), which remove peptide fragments of topoisomerases I and II, respectively, and the Artemis and Metnase endonucleases, which can trim damaged overhangs of diverse structure. TDP1 as well as APE1 can remove 3'-phosphoglycolates and other 3' blocks, while CtIP appears to provide an alternative pathway for topoisomerase II fragment removal. Ku, a core DSB joining protein, can cleave abasic sites near DNA ends. The downstream processes of patching and ligation are tolerant of residual damage, and can sometimes proceed without complete damage removal. Despite these redundant pathways for resolution, damaged ends appear to be a significant barrier to rejoining, and their resolution may be a rate-limiting step in repair of some DSBs..
Identifiers
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.