Site-specific mutagenesis using a gapped duplex vector: A study of translesion synthesis past 8-oxodeoxyguanosine in E. coli

Moriya, Masaaki; Ou, Chin Yih; Bodepudi, Veeraiah; Johnson, Francis; Takeshita, Masaru; Grollman, Arthur P.

doi:10.1016/0921-8777(91)90067-y

Cited by 334 publications

(190 citation statements)

References 18 publications

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“…Loeb and co-workers have clearly shown that while this tandem double mutation, a hallmark of damage to DNA by UV irradiation, is not produced by DNA polymerases or viral reverse transcriptases or by exposure to chemical carcinogens, it can be caused by oxidative damage to DNA Tkeshelashvili et al, 1993). G:C to C:G and G:C to T:A transversions, which were also found to be present at relatively high frequencies in the lung cancers of our non-smoker cohort, are also known to be induced by reactive oxygen species in certain circumstances (Moriya et al, 1991;McBride, 1992). The present findings suggest that oxygen radical species, which can be generated by various mechanisms, including normal cellular processes (Fridovich, 1983), might have a role in the development of lung cancers.…”

Section: Discussionsupporting

confidence: 54%

p53 Mutations in non-small-cell lung cancers occurring in individuals without a past history of active smoking

et al. 1998

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Summary Accumulating evidence suggests that the p53 gene is a good target for molecular epidemiological studies. We previously reported an association between the presence of p53 mutations and lifetime cigarette consumption. Although over 675 p53 mutations have been reported in lung cancers in the literature thus far, very little is known about the nature of such changes in lung cancers in the absence of a smoking background. In the present study, we therefore analysed 69 non-small-cell lung cancer specimens from individuals without any history of active smoking and identified p53 mutations in 26% of the cases. Statistical analysis of the present cohort of non-smokers also showed absence of significant relationship between p53 mutations and age, sex, histological type or disease stage. Comparison of mutational spectra between the present results in non-smokers and previously reported mutations in smokers clearly demonstrated G:C to T:A transversions to be significantly less frequent in non-smokers than in smokers (OR 5.35, 95% Cl 1.77-16.12). Interestingly, G:C to C:G and G:C to A:T mutations were also observed in tumours of non-smokers at similar frequencies to G:C to T:A mutations, suggesting that these mutations can occur relatively frequently in the absence of active smoking. This study is, to our knowledge, the largest so far analysing a welldefined cohort of non-smokers in a single laboratory.

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Section: Discussionsupporting

confidence: 54%

p53 Mutations in non-small-cell lung cancers occurring in individuals without a past history of active smoking

et al. 1998

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“…OH-modi®ed DNA bases, including 8 hydroxydeoxyguanosine (Kuchino et al, 1987;Shibutani et al, 1991;Wood et al, 1990;Moriya et al, 1991;Cheng et al, 1992;Moriya, 1993), cytosine glycol (Hayes et al, 1988), thymine glycol (Basu et al, 1989), and 8 hydroxydeoxyadenosine (Guschlbauer et al, 1991), to mispair with each of the four DNA bases. The spectrum of mutations observed in our .…”

Section: Discussionmentioning

confidence: 99%

Stimulated human leukocytes cause activating mutations in the K-ras proto-oncogene

et al. 1997

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“…Among the numerous DNA lesions formed under conditions of oxidative stress, 7, 8-dihydro-8-oxoguanine (8-oxoG) is notable as it is mutagenic if not repaired [1][2][3][4] where its persistence in the genome can lead to a number of pathological states. The primary means to remove 8-oxoG from DNA is via the action of N-glycosylases that participate in the base excision repair (BER) pathway.…”

Section: Introductionmentioning

confidence: 99%

Translocation of human ribosomal protein S3 to sites of DNA damage is dependant on ERK-mediated phosphorylation following genotoxic stress

2007

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Besides its role in translation and ribosome maturation, human ribosomal protein S3 (hS3) is implicated in DNA damage recognition as reflected by its affinity for abasic sites and 7, 8-dihydro-8-oxoguanine (8-oxoG) residues in DNA in vitro. Here, we demonstrate that hS3 is capable of carrying out both roles by its ex vivo translocation from the cytoplasm to the nucleus as a consequence of genotoxic stress. The translocation of hS3 is dependent on ERK1/2-mediated phosphorylation of a threonine residue (T42) of hS3. Two different ectopically expressed site-directed mutants of T42 failed to respond to conditions of genotoxic stress, thus providing a link between DNA damage and ERK1/2 dependent phosphorylation of hS3. Lastly, hS3 was traced in exposed cells to its colocalization with 8-oxoG foci, raising the possibility that hS3 is a member of a cellular DNA damage response pathway that results in its interaction with sites of DNA damage.

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Site-specific mutagenesis using a gapped duplex vector: A study of translesion synthesis past 8-oxodeoxyguanosine in E. coli

Cited by 334 publications

References 18 publications

p53 Mutations in non-small-cell lung cancers occurring in individuals without a past history of active smoking

p53 Mutations in non-small-cell lung cancers occurring in individuals without a past history of active smoking

Stimulated human leukocytes cause activating mutations in the K-ras proto-oncogene

Translocation of human ribosomal protein S3 to sites of DNA damage is dependant on ERK-mediated phosphorylation following genotoxic stress

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