期刊
MUTAGENESIS
卷 21, 期 3, 页码 173-178出版社
OXFORD UNIV PRESS
DOI: 10.1093/mutage/gel020
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资金
- Medical Research Council [G0700730] Funding Source: Medline
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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