ArticleChemical research in toxicology2013
Replication across regioisomeric ethylated thymidine lesions by purified DNA polymerases.
Article in Chemical research in toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Metabolic Activation and DNA Interactions of CarcinogenicInternational journal of molecular sciences · 2022Review
- Site-Specific Synthesis of Oligonucleotides Containing 6-Oxo-MChemical research in toxicology · 2021Article
- Mammalian DNA Polymerase Kappa Activity and Specificity.Molecules (Basel, Switzerland) · 2019Review
- Synthesis of stable azide and alkyne functionalized phosphoramidite nucleosides.Tetrahedron letters · 2019Article
- Mechanism of DNA alkylation-induced transcriptional stalling, lesion bypass, and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- DNA Polymerase ν Rapidly Bypasses OChemical research in toxicology · 2016Article
- Replicative Bypass of OChemical research in toxicology · 2016Article
- Lesion Orientation ofChemical science · 2016Article
- In Vitro Lesion Bypass Studies of O(4)-Alkylthymidines with Human DNA Polymerase η.Chemical research in toxicology · 2016Article
- DNA Polymerases η and ζ Combine to Bypass O(2)-[4-(3-Pyridyl)-4-oxobutyl]thymine, a DNA Adduct Formed from Tobacco Carcinogens.Chemical research in toxicology · 2016Article
- Mass Spectrometry-Based Quantitative Strategies for Assessing the Biological Consequences and Repair of DNA Adducts.Accounts of chemical research · 2016Review
- Cytotoxic and mutagenic properties of O4-alkylthymidine lesions in Escherichia coli cells.Nucleic acids research · 2015Article
- Mass spectrometry for the assessment of the occurrence and biological consequences of DNA adducts.Chemical Society reviews · 2015Review
- Transcriptional bypass of regioisomeric ethylated thymidine lesions by T7 RNA polymerase and human RNA polymerase II.Nucleic acids research · 2014Article
- Cytotoxic and mutagenic properties of regioisomeric O²-, N3- and O⁴-ethylthymidines in bacterial cells.Carcinogenesis · 2014Article
- Fragmentation of electrospray-produced deprotonated ions of oligodeoxyribonucleotides containing an alkylated or oxidized thymidine.Journal of the American Society for Mass Spectrometry · 2014Article
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
Causal links exist between smoking cigarettes and cancer development. Some genotoxic agents in cigarette smoke are capable of alkylating nucleobases in DNA, and higher levels of ethylated DNA lesions were observed in smokers than in nonsmokers. In this study, we examined comprehensively how the regioisomeric O(2)-, N3-, and O(4)-ethylthymidine (O(2)-, N3-, and O(4)-EtdT, respectively) perturb DNA replication mediated by purified human DNA polymerases (hPols) η, κ, and ι, yeast DNA polymerase ζ (yPol ζ), and the exonuclease-free Klenow fragment (Kf(-)) of Escherichia coli DNA polymerase I. Our results showed that hPol η and Kf(-) could bypass all three lesions and generate full-length replication products, whereas hPol ι stalled after inserting a single nucleotide opposite the lesions. Bypass conducted by hPol κ and yPol ζ differed markedly among the three lesions. Consistent with its known ability to efficiently bypass the minor groove N(2)-substituted 2'-deoxyguanosine lesions, hPol κ was able to bypass O(2)-EtdT, though it experienced great difficulty in bypassing N3-EtdT and O(4)-EtdT. yPol ζ was only modestly blocked by O(4)-EtdT, but the polymerase was strongly hindered by O(2)-EtdT and N3-EtdT. LC-MS/MS analysis of the replication products revealed that DNA synthesis opposite O(4)-EtdT was highly error-prone, with dGMP being preferentially inserted, while the presence of O(2)-EtdT and N3-EtdT in template DNA directed substantial frequencies of misincorporation of dGMP and, for hPol ι and Kf(-), dTMP. Thus, our results suggested that O(2)-EtdT and N3-EtdT may also contribute to the AT → TA and AT → GC mutations observed in cells and tissues of animals exposed to ethylating agents.
Indexed as
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.