ReviewFree radical biology & medicine2017
Formation and processing of DNA damage substrates for the hNEIL enzymes.
Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 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
72 citing papers in PubMed, 120 citations in OpenAlex.
- Nanopore Sequencing Reveals rRNA Modification Changes in Human Cells Experiencing Oxidative or Inflammatory Stress.ACS chemical biology · 2026Article
- Hemin Recapitulates the Labile Iron Pool in the Cellular Fenton Reaction with DNA.Chemical research in toxicology · 2026Article
- DamageFormer: a damage-aware multimodal deep learning framework for DNA lesion identification from nanopore sequencing.bioRxiv : the preprint server for biology · 2026Article
- Single-Molecule Chemistry Part II: Pathway Analysis of the Oxidation of Guanine to 8-Oxo-7,8-dihydroguanosine in an Oligonucleotide Hybrid.Molecules (Basel, Switzerland) · 2026Article
- Probing the epitranscriptome and RNA damage with nanopore direct RNA sequencing.RNA (New York, N.Y.) · 2026Review
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Base excision repair within structure-forming repeat sequences and its impact on cancer and other diseases.NAR cancer · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Crosslinking pathways, dynamics, and kinetics between guanosine and lysine following one- versus two-electron oxidation of guanosine.Nucleic acids research · 2025Article
- Why the ROS matters: One-electron oxidants focus DNA damage and repair on G-quadruplexes for gene regulation.DNA repair · 2025Review
- Hole Transfer and the Resulting DNA Damage.Biomolecules · 2024Review
- COProceedings of the National Academy of Sciences of the United States of America · 2024Article
- CObioRxiv : the preprint server for biology · 2024Article
- An Insight into the Mechanism of DNA Cleavage by DNA Endonuclease from the Hyperthermophilic ArchaeonInternational journal of molecular sciences · 2024Article
- The Influence of 2'-Deoxyguanosine Lesions on the Electronic Properties ofMolecules (Basel, Switzerland) · 2024Review
- Review
- Repair and DNA Polymerase Bypass of Clickable Pyrimidine Nucleotides.Biomolecules · 2024Article
- The Influence of Clustered DNA Damage Containing Iz/Oz andMolecules (Basel, Switzerland) · 2024Article
- The Influence of Oxidized Imino-Allantoin in the Presence ofInternational journal of molecular sciences · 2024Article
12 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are harnessed by the cell for signaling at the same time as being detrimental to cellular components such as DNA. The genome and transcriptome contain instructions that can alter cellular processes when oxidized. The guanine (G) heterocycle in the nucleotide pool, DNA, or RNA is the base most prone to oxidation. The oxidatively-derived products of G consistently observed in high yields from hydroxyl radical, carbonate radical, or singlet oxygen oxidations under conditions modeling the cellular reducing environment are discussed. The major G base oxidation products are 8-oxo-7,8-dihydroguanine (OG), 5-carboxamido-5-formamido-2-iminohydantoin (2Ih), spiroiminodihydantoin (Sp), and 5-guanidinohydantoin (Gh). The yields of these products show dependency on the oxidant and the reaction context that includes nucleoside, single-stranded DNA (ssDNA), double-stranded DNA (dsDNA), and G-quadruplex DNA (G4-DNA) structures. Upon formation of these products in cells, they are recognized by the DNA glycosylases in the base excision repair (BER) pathway. This review focuses on initiation of BER by the mammalian Nei-like1-3 (NEIL1-3) glycosylases for removal of 2Ih, Sp, and Gh. The unique ability of the human NEILs to initiate removal of the hydantoins in ssDNA, bulge-DNA, bubble-DNA, dsDNA, and G4-DNA is outlined. Additionally, when Gh exists in a G4 DNA found in a gene promoter, NEIL-mediated repair is modulated by the plasticity of the G4-DNA structure provided by additional G-runs flanking the sequence. On the basis of these observations and cellular studies from the literature, the interplay between DNA oxidation and BER to alter gene expression is discussed.
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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.