Mutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
Excision repair of DNA base damage in human cells treated with the chemical carcinogen 4-nitroquinoline 1-oxide
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Cited by (77)
P-TEFb Activation by RBM7 Shapes a Pro-survival Transcriptional Response to Genotoxic Stress
2019, Molecular CellCitation Excerpt :Because UV irradiation yields RNA-protein crosslinks immediately and thus prior to DDR activation, we instead employed its mimetic, 4-NQO. Notably, 4-NQO metabolite 4-hydroxyaminoquinolone 1-oxide forms bulky DNA adducts on purines, which are removed by nucleotide excision repair (NER) (Ikenaga et al., 1977). Consistent with the previous report (Lubas et al., 2015), RBM7 bound directly a diverse set of RNAs, including genic, intergenic, and non-coding RNAs (ncRNAs) (Figures 1A, S1A, and S1B; Table S1A).
Interplay of DNA repair, homologous recombination, and DNA polymerases in resistance to the DNA damaging agent 4-nitroquinoline-1-oxide in Escherichia coli
2010, DNA RepairCitation Excerpt :NQO exposure may also cause DSBs when replication forks encounter single-strand nicks or gaps formed during repair of NQO-induced lesions. In E. coli and other organisms the major pathway for repair of NQO-induced DNA lesions is nucleotide excision repair (NER) [9–12]. During NER, the single-strand of DNA immediately surrounding the lesion is excised and the resulting gap is filled in, usually by Pol I [13,14].
Three measures of mutagen sensitivity in a cancer-free population
1999, Cancer Genetics and CytogeneticsThe analysis of DNA adduct formation, removal and persistence in the common mussel Mytilus edulis exposed to 4-nitroquinoline 1-oxide
1998, Mutation Research - Fundamental and Molecular Mechanisms of MutagenesisThe repair of large DNA adducts in mammalian cells
1992, Mutation Research-DNA Repair