Chan Katie K L, Zhang Qiu-Mei, Dianov Grigory L
Radiation and Genome Stability Unit, Medical Research Council Harwell, Oxfordshire, UK.
Mutagenesis. 2006 May;21(3):173-8. doi: 10.1093/mutage/gel020. Epub 2006 Apr 13.
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.
在哺乳动物细胞中，碱基切除修复（BER）是参与去除非大块损伤核苷酸的主要修复途径。BER的保真度取决于聚合步骤，在该步骤中，主要的BER DNA聚合酶（Polβ）必须将正确的沃森-克里克碱基配对核苷酸掺入一个核苷酸修复缺口。最近的研究表明，癌细胞中常见的一些Polβ变体的表达或野生型Polβ蛋白表达的变化，可导致DNA修复合成错误，并赋予细胞突变表型。
