Review
doi: 10.1093/mutage/gel020.
Epub 2006 Apr 13.
Base excision repair fidelity in normal and cancer cells
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- PMID: 16613912
- DOI: 10.1093/mutage/gel020
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Review
Base excision repair fidelity in normal and cancer cells
Mutagenesis.
2006 May.
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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