ArticleBiochemistry2008
Efficient removal of formamidopyrimidines by 8-oxoguanine glycosylases.
Article in Biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Hemin Recapitulates the Labile Iron Pool in the Cellular Fenton Reaction with DNA.Chemical research in toxicology · 2026Article
- Assessment of DNA Variations From Two In Vivo Skeletal Muscle Disorder Mouse Models Using Complementary Square-Wave Voltammetry and LC-MS/MS Analysis.Chembiochem : a European journal of chemical biology · 2026Article
- OGG1 and MUTYH DNA Glycosylases, the Dynamic Duo Against 8-Oxoguanine DNA Lesion: Structure, Regulation, and Novel Emerging Roles.Biomolecules · 2026Review
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- Dynamic genome-wide mapping reveals how chromatin context shapes OGG1-mediated repair and related mutagenesis in human cells.Nucleic acids research · 2025Article
- Telomeric DNA damage landscapes distinguish oxidative from inflammatory cellular stress.Nucleic acids research · 2025Article
- Unlocking the chemistry facilitated by enzymes that process nucleic acids using quantum mechanical and combined quantum mechanics-molecular mechanics techniques.Pure and applied chemistry. Chimie pure et appliquee · 2025Review
- Promoter dependent RNA polymerase II bypass of the epimerizable DNA lesion, Fapy•dG and 8-Oxo-2'-deoxyguanosine.Nucleic acids research · 2024Article
- Probing the Conformational Restraints of DNA Damage Recognition with β-L-Nucleotides.International journal of molecular sciences · 2024Article
- Sequencing for oxidative DNA damage at single-nucleotide resolution with click-code-seq v2.0.Chemical communications (Cambridge, England) · 2023Article
- Structural Dynamics of a Common Mutagenic Oxidative DNA Lesion in Duplex DNA and during DNA Replication.Journal of the American Chemical Society · 2022Article
- Dynamic features of human mitochondrial DNA maintenance and transcription.Frontiers in cell and developmental biology · 2022Review
- Synthesis of Oligonucleotides Containing the NChemistry (Weinheim an der Bergstrasse, Germany) · 2020Article
- The genomics of oxidative DNA damage, repair, and resulting mutagenesis.Computational and structural biotechnology journal · 2020Review
- Inflammation-induced DNA damage, mutations and cancer.DNA repair · 2019Review
- Vitamin E inhibits the UVAI induction of "light" and "dark" cyclobutane pyrimidine dimers, and oxidatively generated DNA damage, in keratinocytes.Scientific reports · 2018Article
- Differential Ability of Five DNA Glycosylases to Recognize and Repair Damage on Nucleosomal DNA.ACS chemical biology · 2017Article
- Synthesis and characterization of oligonucleotides containing a nitrogen mustard formamidopyrimidine monoadduct of deoxyguanosine.Chemical research in toxicology · 2014Article
- Steady-state, pre-steady-state, and single-turnover kinetic measurement for DNA glycosylase activity.Journal of visualized experiments : JoVE · 2013Article
- Inhibition of DNA synthesis facilitates expansion of low-complexity repeats: is strand slippage stimulated by transient local depletion of specific dNTPs?BioEssays : news and reviews in molecular, cellular and developmental biology · 2013Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Under conditions of oxidative stress, the formamidopyrimidine lesions (FapyG and FapyA) are formed in competition with the corresponding 8-oxopurines (OG and OA) from a common intermediate. In order to reveal features of the repair of these lesions, and the potential contribution of repair in mitigating or exacerbating the mutagenic properties of Fapy lesions, their excision by three glycosylases, Fpg, hOGG1 and Ntg1, was examined in various base pair contexts under single-turnover conditions. FapyG was removed at least as efficiently as OG by all three glycosylases. In addition, the rates of removal of FapyG by Fpg and hOGG1 were influenced by their base pair partner, with preference for removal when base paired with the correct Watson-Crick partner C. With the FapyA lesion, Fpg and Ntg1 catalyze its removal more readily than OG opposite all four natural bases. In contrast, the removal of FapyA by hOGG1 was not as robust as FapyG or OG, and was only significant when the lesion was paired with C. The discrimination by the various glycosylases with respect to the opposing base was highly dependent on the identity of the lesion. OG induced the greatest selectivity against its removal when part of a promutagenic base pair. The superb activity of the various OG glycosylases toward removal of FapyG and FapyA in vitro suggests that these enzymes may act upon these oxidized lesions in vivo. The differences in the activity of the various glycosylases for removal of FapyG and FapyA compared to OG in nonmutagenic versus promutagenic base pair contexts may serve to alter the mutagenic profiles of these lesions in vivo.
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