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1                    The results showed that 8-hydroxyguanine (8-OH-Gua) and 2,6-diamino-4-hydroxy-5-fo
2 group B gene plays a role in the repair of 8-hydroxyguanine (8-OH-Gua) in transcription-coupled and n
3                                            8-hydroxyguanine (8-OH-Gua) is one of many lesions generat
4 amino-5-formamidopyrimidine (FapyAde), and 8-hydroxyguanine (8-OH-Gua) was observed among 17 lesions
5                     For example, mutagenic 8-hydroxyguanine (8-OH-Gua) was reduced approximately 50%
6 tic studies revealed efficient excision of 8-hydroxyguanine (8-OH-Gua), 2,6-diamino-4-hydroxy-5-forma
7 (FapyGua) from DNA with no specificity for 8-hydroxyguanine (8-OH-Gua).
8 te-stage AD (LAD) brain show elevations of 8-hydroxyguanine (8-OHG), 8-hydroxyadenine (8-OHA), 5-hydr
9                               Formation of 8-hydroxyguanine (8-OHG), a mutagenic base which is a mark
10 humans, the oxidatively induced DNA lesion 8-hydroxyguanine (8-oxoG) is removed from DNA by hOgg1, a
11            The major oxidative DNA lesion, 8-hydroxyguanine (8-oxoG), is increased in breast cancer,
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                                      Also, 8-hydroxyguanine accumulated more in CSB null and motif VI
15  protein is involved in cellular repair of 8-hydroxyguanine, an abundant lesion in oxidatively damage
16 ations of the mutagenic base modifications 8-hydroxyguanine and 8-hydroxyadenine.
17 that can suppress the mutagenic effects of 8-hydroxyguanine by catalyzing its removal from oxidized D
18  not attributable to lower levels of human 8-hydroxyguanine DNA glycosylase, the base excision repair
19 se that removes oxidized guanine from DNA, 8-hydroxyguanine-DNA glycosylase (OGG1).
20 , 8-hydroxyadenine, 5-hydroxycytosine, and 8-hydroxyguanine) examined by gas chromatography/mass spec
21  from misincorporation of adenine opposite 8-hydroxyguanine in one strand and 6-hydroxylaminopurine o
22 d motif V/VI mutants had lower activity of 8-hydroxyguanine incision in DNA than wild type cells.
23                                            8-Hydroxyguanine is a mutagenic base lesion produced by re
24       These ROS resulted in an increase in 8-hydroxyguanine lesions and DNA fragmentation that signal
25 absence of Ogg1 activity and indicate that 8-hydroxyguanine lesions most likely do not cause V gene m
26 d type mice were significantly higher than 8-hydroxyguanine levels.
27 ast, Ntg1 and Ntg2 proteins do not release 8-hydroxyguanine or 8-hydroxyadenine from gamma-irradiated
28 g1(-/-) clones, which would be expected if 8-hydroxyguanine remained in the DNA.
29 sites; however, no significant excision of 8-hydroxyguanine was observed.
30 trations of 8-hydroxypurine lesions (e.g., 8-hydroxyguanine) were substantially higher for the older

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