Chemical biology of mutagenesis and DNA repair: cellular responses to DNA alkylation

被引:215
作者
Shrivastav, Nidhi [1 ,2 ]
Li, Deyu [1 ,2 ]
Essigmann, John M. [1 ,2 ]
机构
[1] MIT, Dept Biol Engn, Cambridge, MA 02139 USA
[2] MIT, Dept Chem, Cambridge, MA 02139 USA
基金
美国国家卫生研究院;
关键词
NUCLEOTIDE EXCISION-REPAIR; METHYL-N-NITROSOUREA; SITE-SPECIFIC MUTAGENESIS; HUMAN 3-METHYLADENINE DNA; ESCHERICHIA-COLI; DEOXYRIBONUCLEIC-ACID; IN-VITRO; ADAPTIVE RESPONSE; OXIDATIVE DEMETHYLATION; LIPID-PEROXIDATION;
D O I
10.1093/carcin/bgp262
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The reaction of DNA-damaging agents with the genome results in a plethora of lesions, commonly referred to as adducts. Adducts may cause DNA to mutate, they may represent the chemical precursors of lethal events and they can disrupt expression of genes. Determination of which adduct is responsible for each of these biological endpoints is difficult, but this task has been accomplished for some carcinogenic DNA-damaging agents. Here, we describe the respective contributions of specific DNA lesions to the biological effects of low molecular weight alkylating agents.
引用
收藏
页码:59 / 70
页数:12
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