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1 ivity in AHR-proficient cells incubated with beta-naphthoflavone.
2 igand of the aryl hydrocarbon receptor (AHR) beta-naphthoflavone.
3 enyl (PCB-126), indolo[3,2-b]-carbazole, and beta-naphthoflavone.
4 ibits high-affinity binding to [(3)H]TCDD or beta-naphthoflavone.
5 llifish all fail to bind [(3)H]TCDD or [(3)H]beta-naphthoflavone.
6 tert-butylhydroxyanisole, sulforaphane, and beta-naphthoflavone.
7 hanced 11-fold in the presence of the ligand beta-naphthoflavone.
8 ected by the arylhydrocarbon receptor ligand beta-naphthoflavone.
10 th a potency five times greater than that of beta-naphthoflavone, a prototypical synthetic AHR ligand
12 s resulted in the conversion of AhR agonists beta-naphthoflavone and 3-methylcholanthrene, respective
14 as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.
15 II enzymes, such as tert-butylhydroquinone, beta-naphthoflavone, and sulforaphane, significantly inc
16 vity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl hydroquinone red
18 onsiveness; some groups were pretreated with beta-naphthoflavone (beta NF), a cytochrome P450 1A indu
22 phorylation, whereas the addition of tBHQ or beta-naphthoflavone (betaNF) led to a persistent stimula
23 Induction of P450s by phenobarbital (PB), beta-naphthoflavone (betaNF), or clofibrate in a mouse m
24 ered to naive, phenobarbital (PB)-induced or beta-naphthoflavone (betaNF)-induced mice, and the level
26 arget genes, C57BL/6J mice were treated with beta-naphthoflavone (BNF), a known AhR ligand, and genom
31 cells treated with tert-butylhydroquinone or beta-naphthoflavone by a post-transcriptional mechanism.
32 h the prooxidants tert-butylhydroquinone and beta-naphthoflavone, cellular UGT1A1 glucuronidation act
37 studies from our laboratory showed that the beta-naphthoflavone-inducible cytochrome P4501A1 is targ
39 ecently, we showed that the major species of beta-naphthoflavone-inducible rat liver mitochondrial P4
40 o generate K-ras(V12)/Cre mice, which showed beta-naphthoflavone-induction of Cre-mediated LoxP recom
41 ves preferentially inhibited P450 1A2, while beta-naphthoflavone-like flavone derivatives showed sele
42 expression in Huh.8 cells by TCDD but not by beta-naphthoflavone or 3-methylcholanthrene was signific
43 dly increased in livers of rats treated with beta-naphthoflavone or 4-methyl-5-pyrazinyl-3H-1,2-dithi
46 2 cells treated with tert-butylhydroquinone, beta-naphthoflavone, or 12-O-tetradecanoylphorbol-13-ace
47 were pretreated with typical P450 inducers (beta-naphthoflavone, phenobarbital (PB), Aroclor 1254, i
48 asional intestinal adenomas were observed in beta-naphthoflavone-treated K-ras(V12)/Cre mice aged up
51 ract obtained from Hepa 1 cells treated with beta-naphthoflavone using an anti-AhR polyclonal antibod
52 y inducing AHR transcriptional activity with beta-naphthoflavone via intraperitoneal injection, and m
55 ich develop adenomas after administration of beta-naphthoflavone, were crossed with mice with conditi
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