期刊
TRENDS IN BIOCHEMICAL SCIENCES
卷 37, 期 4, 页码 162-172出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2011.12.002
关键词
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资金
- NIH from the National Institute of Environmental Health Sciences (NIEHS) [Z01-ES050158, Z01-ES050159]
- NIH [ES017476]
The expansion of trinucleotide repeat (TNR) sequences in human DNA is considered to be a key factor in the pathogenesis of more than 40 neurodegenerative diseases. TNR expansion occurs during DNA replication and also, as suggested by recent studies, during the repair of DNA lesions produced by oxidative stress. In particular, the oxidized guanine base 8-oxoguanine within sequences containing CAG repeats may induce formation of pro-expansion intermediates through strand slippage during DNA base excision repair (BER). In this article, we describe how oxidized DNA lesions are repaired by BER and discuss the importance of the coordinated activities of the key repair enzymes, such as DNA polymerase beta, flap endonuclease 1 (FEN1) and DNA ligase, in preventing strand slippage and TNR expansion.
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