Analysis of cell cycle-dependent base excision repair by a novel direct method for detecting the intracellular AP sites

利用一种新的核内脱碱基位点检测系统研究了甲基化碱基损伤的细胞周期依赖性碱基切除修复。在polβ-KO MEF中，甲基化碱基的去除明显慢于野生型，特别是在G1期，这表明缺乏抑制了糖基化酶活性，以绕过有害中间体AP位点的积累。

The cell cycle dependent base excision repair of methylated base damage was investigated using a novel assay system for the detection of intranuclear abasic sites. In polβ-KO MEF, the removal of methylated bases was significantly slower than wild type especially in G1 phase, suggesting the lack suppressed the glycosylase activity to bypass the accumulation of hazardous intermediate, AP sites.