Carcinogenesis, Vol. 22, No. 7, 987-998,
July 2001
© 2001 Oxford University Press
COMMENTARY |
Base excision repair in a network of defence and tolerance
Institute of Cancer Research and Molecular Biology, Norwegian University of Science and Technology, N-7489 Trondheim, Norway
Abbreviations: AP sites,abasic sites; BER,base excision repair; dRP,deoxyribose 5-phosphate; HNPCC,hereditary non-polyposis colon cancer; MMR,mismatch repair; MPG,methylpurine-DNA glycosylase; NER,nucleotide excision repair; PCNA,proliferating cell nuclear antigen; Pol,DNA polymerase; RFC,replication factor C; TDG,thymine/uracil mismatch glycosylase; TLS,translesion DNA synthesis; UDG,uracil-DNA glycosylase; UNG,uracil-DNA glycosylase.
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Introduction |
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Survival of a species depends on balanced generation of genetic variation but at the same time on the protection of the genome from changes that cause disease and fitness reduction. DNA repair pathways limit mutations but do not totally eliminate them. In fact, some DNA repair pathways are error prone. DNA repair thus has a central function not only in protecting the genome, but also in the generation of genetic diversity. Expression of DNA repair proteins is subject to a delicate balance where both too few and too many of a type may result in increased cytotoxicity and/or mutation (1–4). DNA repair is integrated with transcription, replication, cell cycle control and apoptosis in complex networks (5), a full discussion of which is beyond the scope of this article, and our abilities. While DNA repair is an ancient and conserved defence mechanism, various pathways, and
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Sources of damage to the genome |
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Base excision repair |
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Knockout mice deficient in BER |
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DNA glycosylases may have overlapping functions in BER and other DNA repair pathways also complement BER |
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Are endogenous damage and cellular transactions major causes of mutations and cancer? |
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Mutation and promotion in cancer development
Error-prone DNA polymerases in generation of endogenous mutations
Does transcription across non-blocking DNA lesions contribute to mutations?
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Is a major role of BER to protect the long-term integrity of the genome? |
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Future perspectives |
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Notes |
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Acknowledgments |
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References |
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