Site-specific mutagenesis using a gapped duplex vector: A study of translesion synthesis past 8-oxodeoxyguanosine in E. coli
References (31)
- et al.
An activity of Escherichia coli that specifically removes 8-hydroxyguanine residues from DNA
Mutation Res.
(1991) - et al.
Mutagenesis by single site-specific arylamine-DNA adducts
J. Biol. Chem.
(1989) - et al.
DNA replication
J. Biol. Chem.
(1988)- et al.
Evaluation of the new system (umu-test) for the detection of environmental mutagens and carcinogens
Mutation Res.
(1985) - et al.
Oligodeoxynucleotides containing synthetic abasic sites
J. Biol. Chem.
(1987) - et al.
Frequency and spectrum of mutations produced by a single cis-syn thymine-thymine cyclobutane dimer in a single-stranded vector
- et al.
SOS-dependent replication past a single trans - syn T-T cyclobutane dimer gives a different mutation spectrum and increased error rate compared to replication past this lesion in uninduced cells
J. Bacteriol.
(1990) - et al.
An improved method for the preparation of the phosphoramidites of modified 2′-deoxynucleotides: incorporation of 8-oxo-2′-deoxyguanosine into synthetic oligomers
Nucleosides and Nucleotides
(1991) - et al.
Single adduct mutagenesis: strong effect of the position of a single acetylaminofluorecene adduct within a mutation hot spot
Formation of an 8-hydroxyguanine moiety in deoxyribonucleic acid on γ-irradiation in aqueous solution
Biochemistry
Hydroxylation of deoxyguanosine at the C-8 position by ascorbic acid and other reducing agents
Nucleic Acid Res.
DNA damage induced by asbestos in the presence of hydrogen peroxide
Gann
Formation of 8-hydroxyguanine residues in DNA by X-irradiation
Gann
Formation of 8-hydroxyguanine moiety in cellular DNA by agents producing oxygen radicals and evidence for its repair
Carcinogenesis
Cited by (343)
PMAP-23 triggers cell death by nitric oxide-induced redox imbalance in Escherichia coli
2019, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :When the oxidation of DNA is not repaired, this base lesion can be bypassed by DNA polymerases and originates mutations. DNA oxidation eventually leads to DNA damage such as DNA strand break [54,55]. Based on the above results, we hypothesized that oxidative stress may be the cause of genotoxicity of PMAP-23, hence DNA strand break was evaluated.
Review of the evidence for thresholds for DNA-Reactive and epigenetic experimental chemical carcinogens
2019, Chemico-Biological InteractionsCitation Excerpt :Moreover, it appears that the cell can accommodate a level of oxidative damage since that is a common background alteration, arising from cellular metabolic processes [61,206,209]. Moreover, oxidative lesions in DNA, are only weakly promutagenic [210,211], which may account for the observation that the carcinogen p-dichlorobenzene, which induces oxidative stress, has activity as a promoting agent, but not an initiating agent [212]. Some epigenetic carcinogens engage in receptor binding which can mediate their effects in a variety of ways.
The roles of human MTH1, MTH2 and MTH3 proteins in maintaining genome stability under oxidative stress
2018, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisSingle-Cell Analysis of Human Pancreas Reveals Transcriptional Signatures of Aging and Somatic Mutation Patterns
2017, CellCitation Excerpt :The pancreas-specific signature S1 was characterized by C > A substitutions, with C > G and C > T substitutions at progressively lower rates. C > A and C > G substitutions are attributed to oxidation of the guanine base, creating 8-Oxo-2′-deoxyguanosine (8-Oxo) that mispairs with adenine and can be further oxidized to mispair with guanine (Moriya et al., 1991; Kino and Sugiyama, 2005), whereas C > T substitutions are attributed to oxidation of the cytosine base (Kreutzer and Essigmann, 1998). Consistent with oxidation of guanosine driving the mutational signature of β cells, 8-hydroxyguanosine levels were markedly elevated in the DNA of β cells compared to non-islet cells, while only modestly elevated in RNA (Figure 5).