期刊
JOURNAL OF NUCLEIC ACIDS
卷 2010, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.4061/2010/543531
关键词
-
资金
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- Central Research Institute of the Electric Power Industry in Japan
- Japan Space Forum
The cytotoxic effects of alkylating agents are strongly attenuated by cellular DNA repair processes, necessitating a clear understanding of the repair mechanisms. Simple methylating agents form adducts at N-and O-atoms. N-methylations are removed by base excision repair, AlkB homologues, or nucleotide excision repair (NER). O-6-methylguanine (MeG), which can eventually become cytotoxic and mutagenic, is repaired by O-6-methylguanine-DNA methyltransferase, and O(6)MeG: T mispairs are recognized by the mismatch repair system (MMR). MMR cannot repair the O(6)MeG/T mispairs, which eventually lead to double-strand breaks. Bifunctional alkylating agents form interstrand cross-links (ICLs) which are more complex and highly cytotoxic. ICLs are repaired by complex of NER factors (e.g., endnuclease xeroderma pigmentosum complementation group Fexcision repair cross-complementing rodent repair deficiency complementation group 1), Fanconi anemia repair, and homologous recombination. A detailed understanding of how cells cope with DNA damage caused by alkylating agents is therefore potentially useful in clinical medicine.
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