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Mutagenesis Advance Access originally published online on April 13, 2006
Mutagenesis 2006 21(3):173-178; doi:10.1093/mutage/gel020
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© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org

Base excision repair fidelity in normal and cancer cells

Katie K.L. Chan1, Qiu-Mei Zhang2 and Grigory L. Dianov1,*

1 Radiation and Genome Stability Unit, Medical Research Council Harwell, Oxfordshire OX11 0RD, UK 2 Laboratory of Radiation Biology, Graduate School of Sciences, Kyoto University, Kitashirakawa-Oiwakecho Sakyo-ku, Kyoto 606-8502, Japan

In mammalian cells, base excision repair (BER) is the major repair pathway involved in the removal of non-bulky damaged nucleotides. The fidelity of BER is dependent on the polymerization step, where the major BER DNA polymerase (Pol ß) must incorporate the correct Watson–Crick base paired nucleotide into the one nucleotide repair gap. Recent studies have indicated that expression of some Pol ß variants or changes in expression of wild-type Pol ß protein, frequently found in cancer cells, can lead to DNA repair synthesis errors and confers to cells a mutator phenotype.

*To whom correspondence should be addressed. Tel: +44 1235 841134; Fax: +44 1235 841200; Email: g.dianov{at}har.mrc.ac.uk


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