DNA 聚合酶 β 在 DNA 修复作用中的分子机制  

MOLECULAR MECHANISM OF DNA pol β IN DNA REPAIR

作　　者：郑秀龙[1] 蔡建明[1] 

机构地区：[1]上海第二军医大学放射医学研究所

出　　处：《辐射研究与辐射工艺学报》1997年第3期168-170,174,共4页Journal of Radiation Research and Radiation Processing

基　　金：国家自然科学基金

摘　　要：利用肝癌与正常肝细胞ＤＮＡｐｏｌβ（β酶）活力存在的差别，观察到γ射线照射对β酶活力无明显影响，肝癌细胞的β酶活力仍明显高于正常肝细胞，表明肝癌对照射ＤＮＡ损伤修复合成能力比正常强，其修复作用机制，经用免疫组化和胞浆斑点杂交法研究，显示肝癌细胞β酶活力的增高是由于基因过度表达及其转录（ｍＲＮＡ）水平的增强有关。The difference of DNA pol β activity between hepatoma and hepatocytes was used to observe no obvious influence on their activity after γ irradiation The pol β activity of hepatoma was still greater than normal hepatocytes It showed that the repair synthesis ability to the iradiated DNA damage in hepatoma was greater than normal It was found that the molecular mechanism of pol β was that higher pol β activity in hepatoma was due to its gene over expression and higher transcription (mRNA) level by immunocytochemistry and cytoplasmic dot hybridization investigation

关 键 词：DNA修复 基因表达 MRNA 聚合酶β 肝癌 放射治疗 

分 类 号：R730.55[医药卫生—肿瘤] R735.7[医药卫生—临床医学]