ライフサイエンスコーパス: beta-naphthoflavone

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.

9 AP-1 stimulators, such as beta-naphthoflavone, 3-methylcholanthrene, and tBHQ, sig

10 th a potency five times greater than that of beta-naphthoflavone, a prototypical synthetic AHR ligand

11 Upon treatment with the agonist beta-naphthoflavone, AHR is rapidly associated with the

12 s resulted in the conversion of AhR agonists beta-naphthoflavone and 3-methylcholanthrene, respective

13 in transfected cells that were inducible by beta-naphthoflavone and teri-butyl hydroquinone.

14 ous combinations of the aromatic hydrocarbon beta-naphthoflavone and the azole nocodazole.

15 as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene metabolites.

16 II enzymes, such as tert-butylhydroquinone, beta-naphthoflavone, and sulforaphane, significantly inc

17 vity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl hydroquinone red

18 as disrupted in liver following injection of beta-naphthoflavone (Axin1fl/fl/Cre mice).

19 onsiveness; some groups were pretreated with beta-naphthoflavone (beta NF), a cytochrome P450 1A indu

20 Exposure of HepG2 cells to beta-naphthoflavone (beta-NF) or pyrrolidine dithiocarba

21 Exposure of HepG2 cells to beta-naphthoflavone (beta-NF) resulted in a time- and do

22 Exposure of HepG2 cells to beta-naphthoflavone (beta-NF) results in time- and dose-

23 phorylation, whereas the addition of tBHQ or beta-naphthoflavone (betaNF) led to a persistent stimula

24 Induction of P450s by phenobarbital (PB), beta-naphthoflavone (betaNF), or clofibrate in a mouse m

25 ered to naive, phenobarbital (PB)-induced or beta-naphthoflavone (betaNF)-induced mice, and the level

26 Induction of cytochrome P-450s by beta-naphthoflavone (BN) enhanced CCE measured by Sr(2+)

27 Other well-known Ahr agonists, such as beta-naphthoflavone (BNF), 3,3',4,4',5-pentachlorobiphen

28 arget genes, C57BL/6J mice were treated with beta-naphthoflavone (BNF), a known AhR ligand, and genom

29 ,2-b]carbazole (FICZ), benzo[a]pyrene (BaP), beta-naphthoflavone (BNF), Indigo and Indirubin, reveal

30 Upon exposure to beta-naphthoflavone (BNF), the spheroids showed a marked

31 homologue binds neither [(3)H]TCDD nor [(3)H]beta-naphthoflavone (BNF).

32 atment with a prototypical PAH-type inducer, beta-naphthoflavone (BNF).

33 was markedly enhanced in both cell types by beta-naphthoflavone (BNF).

34 its promoter activity after incubations with beta-naphthoflavone by 5-fold.

35 cells treated with tert-butylhydroquinone or beta-naphthoflavone by a post-transcriptional mechanism.

36 h the prooxidants tert-butylhydroquinone and beta-naphthoflavone, cellular UGT1A1 glucuronidation act

37 was performed with the additional effectors beta-naphthoflavone, flavone, and 4-chromanone.

38 a dioxin analog, and it is not activated by beta-naphthoflavone in the yeast system.

39 re also found localized in mitochondria from beta-naphthoflavone-induced livers.

40 ction of liver homogenate from phenobarbital/beta-naphthoflavone-induced Sprague-Dawley rats.

41 studies from our laboratory showed that the beta-naphthoflavone-inducible cytochrome P4501A1 is targ

42 Recently we showed that the beta-naphthoflavone-inducible liver mitochondrial P450MT

43 ecently, we showed that the major species of beta-naphthoflavone-inducible rat liver mitochondrial P4

44 o generate K-ras(V12)/Cre mice, which showed beta-naphthoflavone-induction of Cre-mediated LoxP recom

45 ves preferentially inhibited P450 1A2, while beta-naphthoflavone-like flavone derivatives showed sele

46 expression in Huh.8 cells by TCDD but not by beta-naphthoflavone or 3-methylcholanthrene was signific

47 dly increased in livers of rats treated with beta-naphthoflavone or 4-methyl-5-pyrazinyl-3H-1,2-dithi

48 plicated in the regulation of other genes by beta-naphthoflavone or oltipraz, were found.

49 ymes were induced in C57 bl/6 mice by either beta-naphthoflavone or phenobarbital.

50 2 cells treated with tert-butylhydroquinone, beta-naphthoflavone, or 12-O-tetradecanoylphorbol-13-ace

51 were pretreated with typical P450 inducers (beta-naphthoflavone, phenobarbital (PB), Aroclor 1254, i

52 asional intestinal adenomas were observed in beta-naphthoflavone-treated K-ras(V12)/Cre mice aged up

53 Clofibrate, 3-methylcholanthrene, or beta-naphthoflavone treatment of male rats or pyridine t

54 After beta-naphthoflavone treatment, K-ras(V12)/Cre/Msh2(-/-)

55 ract obtained from Hepa 1 cells treated with beta-naphthoflavone using an anti-AhR polyclonal antibod

56 y inducing AHR transcriptional activity with beta-naphthoflavone via intraperitoneal injection, and m

57 The endoprotease, which was induced by beta-naphthoflavone, was a dimer of 90 kDa and 40 kDa su

58 Hexachlorobenzene, benzo(a)pyrene, and beta-naphthoflavone were effective AHR agonists in the y

59 ich develop adenomas after administration of beta-naphthoflavone, were crossed with mice with conditi