ArticleBiochemistry2010
Mutagenic potential of DNA glycation: miscoding by (R)- and (S)-N2-(1-carboxyethyl)-2'-deoxyguanosine.
Article in Biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
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
21 citing papers in PubMed.
- A Citrus and Pomegranate Complex Reduces Methylglyoxal in Healthy Elderly Subjects: Secondary Analysis of a Double-Blind Randomized Cross-Over Clinical Trial.International journal of molecular sciences · 2023Trial
- Aldehyde Detoxification in Cancer: Metabolic Guardians of the Genome.Biomolecules · 2026Review
- NScientific reports · 2026Article
- Higher intakes of dietary dicarbonyl compounds are associated with lower risk of cardiovascular disease.European journal of preventive cardiology · 2025Article
- Self-DNA by Activating the CGAS-STING1 Pathway Contributes to the Pathogenesis of Atherosclerosis.Current atherosclerosis reports · 2025Review
- Methylglyoxal mutagenizes single-stranded DNA via Rev1-associated slippage and mispairing.Nucleic acids research · 2025Article
- Methylglyoxal mutagenizes single-stranded DNA via Rev1-associated slippage and mispairing.bioRxiv : the preprint server for biology · 2025Article
- The roles of advanced glycation end products in cardiovascular diseases: from mechanisms to therapeutic strategies.Frontiers in cardiovascular medicine · 2025Review
- An overview on glycation: molecular mechanisms, impact on proteins, pathogenesis, and inhibition.Biophysical reviews · 2024Review
- Glyoxalase I is a novel target for the prevention of metabolic derangement.Pharmacology & therapeutics · 2023Review
- Aldehyde-Associated Mutagenesis─Current State of Knowledge.Chemical research in toxicology · 2023Review
- Article
- Elevated glucose increases genomic instability by inhibiting nucleotide excision repair.Life science alliance · 2021Article
- Non-enzymatic covalent modifications: a new link between metabolism and epigenetics.Protein & cell · 2020Review
- Product Studies and Mechanistic Analysis of the Reaction of Methylglyoxal with Deoxyguanosine.Chemical research in toxicology · 2018Article
- DNA Advanced Glycation End Products (DNA-AGEs) Are Elevated in Urine and Tissue in an Animal Model of Type 2 Diabetes.Chemical research in toxicology · 2017Article
- The Role of Advanced Glycation End-Products in Cancer Disparity.Advances in cancer research · 2017Review
- Glycation Reactivity of a Quorum-Sensing Signaling Molecule.Angewandte Chemie (International ed. in English) · 2016Article
- Characterization of the deoxyguanosine-lysine cross-link of methylglyoxal.Chemical research in toxicology · 2014Article
- Pathological significance of mitochondrial glycation.International journal of cell biology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Elevated circulating glucose resulting from complications of obesity and metabolic disease can result in the accumulation of advanced glycation end products (AGEs) of proteins, lipids, and DNA. The formation of DNA-AGEs assumes particular importance as these adducts may contribute to genetic instability and elevated cancer risk associated with metabolic disease. The principal DNA-AGE, N(2)-(1-carboxyethyl)-2'-deoxyguanosine (CEdG), is formed as a mixture of R and S isomers at both the polymer and monomer levels. In order to examine the miscoding potential of this adduct, oligonucleotides substituted with (R)- and (S)-CEdG and the corresponding triphosphates (R)- and (S)-CEdGTP were synthesized, and base-pairing preferences for each stereoisomer were examined using steady-state kinetic approaches. Purine dNTPs were preferentially incorporated opposite template CEdG when either the Klenow (Kf(-)) or Thermus aquaticus (Taq) polymerases were used. The Kf(-) polymerase preferentially incorporated dGTP, whereas Taq demonstrated a bias for dATP. Kf(-) incorporated purines opposite the R isomer with greater efficiency, but Taq favored the S isomer. Incorporation of (R)- and (S)-CEdGTP only occurred opposite dC and was catalyzed by Kf(-) with equal efficiencies. Primer extension from a 3'-terminal CEdG was observed only for the R isomer. These data suggest CEdG is the likely adduct responsible for the observed pattern of G transversions induced by exposure to elevated glucose or its alpha-oxoaldehyde decomposition product methylglyoxal. The results imply that CEdG within template DNA and the corresponding triphosphate possess different syn/anti conformations during replication which influence base-pairing preferences. The implications for CEdG-induced mutagenesis in vivo are discussed.
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Registered trials
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