Carcinogenesis, Vol. 21, No. 6, 1071-1078,
June 2000
© 2000 Oxford University Press
Commentary |
Nucleic acid sequence and repair: role of adduct, neighbor bases and enzyme specificity
Donner Laboratory, Life Sciences Division, Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA
Abbreviations: AAF, N-acetyl-2-aminofluorene; AF, N-2-aminofluorene; AGT, O6-alkylguanine-DNA alkyltransferase; AP, apurinic/apyrimidinic; APNG, alkylpurine-N-DNA glycosylase; BPDE, benzo[a]pyrene diol epoxide; e6G, O6-ethylguanine; 
A, 1,N6-ethenoadenine; m6G, O6-methylguanine; NER, nucleotide excision repair.
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Historical perspective |
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The study of the role of sequence in base modification was mainly started in the 1980s in terms of sequence selectivity for mutational events (see for example 1–20). These events were generally roduced by environmental agents, such as UV exposure, alkylating agents and aromatic amines, or spontaneously (21). It has since become clear that such events are not totally random but tend to predominate at specific sites in nucleic acids. This type of investigation led to the idea of `targeted' mutation, which was often related to specific cellular changes in function.
At the onset of the interest in how base sequence affected modification, there was also interest in whether the base sequences flanking damage could also influence replication (see for example 22–25) and repair (see for example 7,8,13,26–28). Significant progress in these research areas was accelerated when it became feasible to design and construct synthetic oligonucleotides with site-directed
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Sequence and repair |
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Repair of aromatic amines by NER
Repair of O6-alkylguanine by AGT
Repair of base mismatches
3'-Exonuclease activity of T4 DNA polymerase
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Sequence, modification and repair |
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Sequence, thermodynamic stability and repair |
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Conclusions |
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Notes |
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Acknowledgments |
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References |
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