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2 group B gene plays a role in the repair of 8-hydroxyguanine (8-OH-Gua) in transcription-coupled and n
4 amino-5-formamidopyrimidine (FapyAde), and 8-hydroxyguanine (8-OH-Gua) was observed among 17 lesions
6 tic studies revealed efficient excision of 8-hydroxyguanine (8-OH-Gua), 2,6-diamino-4-hydroxy-5-forma
8 te-stage AD (LAD) brain show elevations of 8-hydroxyguanine (8-OHG), 8-hydroxyadenine (8-OHA), 5-hydr
10 humans, the oxidatively induced DNA lesion 8-hydroxyguanine (8-oxoG) is removed from DNA by hOgg1, a
12 thetic RNA containing the oxidative lesion 8-hydroxyguanine (8-oxoG), suggesting a possible role in r
13 oxidatively modified DNA damage biomarkers 8-hydroxyguanine, 8-hydroxyadenine and 5-hydroxyuracil, co
14 ed a statistically significant increase in 8-hydroxyguanine, a known artifact, and additional artifac
16 protein is involved in cellular repair of 8-hydroxyguanine, an abundant lesion in oxidatively damage
18 that can suppress the mutagenic effects of 8-hydroxyguanine by catalyzing its removal from oxidized D
19 not attributable to lower levels of human 8-hydroxyguanine DNA glycosylase, the base excision repair
21 , 8-hydroxyadenine, 5-hydroxycytosine, and 8-hydroxyguanine) examined by gas chromatography/mass spec
22 from misincorporation of adenine opposite 8-hydroxyguanine in one strand and 6-hydroxylaminopurine o
23 d motif V/VI mutants had lower activity of 8-hydroxyguanine incision in DNA than wild type cells.
26 absence of Ogg1 activity and indicate that 8-hydroxyguanine lesions most likely do not cause V gene m
28 ast, Ntg1 and Ntg2 proteins do not release 8-hydroxyguanine or 8-hydroxyadenine from gamma-irradiated
31 trations of 8-hydroxypurine lesions (e.g., 8-hydroxyguanine) were substantially higher for the older