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Mutagenesis Advance Access published online on April 13, 2006
Mutagenesis, 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
Received February 10, 2006
Revised March 17, 2006
Accepted March 17, 2006

Review

Base excision repair fidelity in normal and cancer cells

Katie K. L. Chan 1, Qiu-Mei Zhang 2, and Grigory L. Dianov 1 *

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

* To whom correspondence should be addressed.
Grigory L. Dianov, E-mail: g.dianov{at}har.mrc.ac.uk


  Abstract

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 {beta}) must incorporate the correct Watson-Crick base paired nucleotide into the one nucleotide repair gap. Recent studies have indicated that expression of some Pol {beta} variants or changes in expression of wild-type Pol {beta} protein, frequently found in cancer cells, can lead to DNA repair synthesis errors and confers to cells a mutator phenotype.


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