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Mitochondrial dysfunction and increased sensitivity to excitotoxicity in mice deficient in DNA mismatch repair

✍ 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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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

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## Abstract Ogg1 DNA repair enzyme recognizes and excises oxidative stress‐caused 8‐hydroxyl‐deoxyguanosine (8‐OHdG) from GC base‐pairs. Ogg1 knockout mice are phenotypically normal, but exhibit elevated levels of 8‐OHdG in nuclear and mitochondrial DNA, as well as moderately elevated mutagenesis a