Mitochondrial dysfunction and increased sensitivity to excitotoxicity in mice deficient in DNA mismatch repair
β Scribed by Simona Francisconi; Mara Codenotti; Giulia Ferrari Toninelli; Daniela Uberti; Maurizio Memo
- Book ID
- 111179558
- Publisher
- John Wiley and Sons
- Year
- 2006
- Tongue
- English
- Weight
- 313 KB
- Volume
- 98
- Category
- Article
- ISSN
- 0022-3042
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π SIMILAR VOLUMES
Together with tolerance to killing induced by methylating agents, loss of mismatch repair (MMR) has previously been found to be associated with hypersensitivity to the DNAcross-linking agent 1-(2-chloroethyl)-3-cyclohexyl-nitrosourea(CCNU) in several human tumor cell lines (Aquilina et al., 1998). H
## Abstract Ogg1 DNA repair enzyme recognizes and excises oxidative stressβcaused 8βhydroxylβdeoxyguanosine (8βOHdG) from GC baseβpairs. Ogg1 knockout mice are phenotypically normal, but exhibit elevated levels of 8βOHdG in nuclear and mitochondrial DNA, as well as moderately elevated mutagenesis a