ライフサイエンスコーパス: alpha-naphthoflavone

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1 structure of human CYP1A1 with the inhibitor alpha-naphthoflavone.

2 pid Nanodiscs, with and without the effector alpha-naphthoflavone.

3 sed by coincubation with the CYP1A inhibitor alpha-naphthoflavone.

4 rd site, distinct from both testosterone and alpha-naphthoflavone.

5 evel of heterotropic stimulation elicited by alpha-naphthoflavone.

6 and (iii) treatment with the AHR antagonist alpha-naphthoflavone.

7 ning steroid hydroxylation or stimulation by alpha-naphthoflavone.

8 de or by the AhR antagonists resveratrol and alpha-naphthoflavone.

9 fluorescent properties of bromocriptine and alpha-naphthoflavone allowed analysis of an initial liga

10 ing purified CYP3A4 and MDZ showed that both alpha-naphthoflavone (alpha-NF) and testosterone affect

11 In the present study, we observed that alpha-naphthoflavone (alpha-NF) exhibited a differential

12 Flavonoids, e.g., 7,8-benzoflavone (alpha-naphthoflavone, alpha NF), have been shown to stim

13 The partial AHR agonist alpha-naphthoflavone (alphaNF) mediates the suppressive,

14 was found to catalyze the 5,6-epoxidation of alpha-naphthoflavone (alphaNF), 1-hydroxylation of pyren

15 The AhR antagonist alpha-naphthoflavone also attenuated B[a]P-7,8-dione-med

16 rate of oxo8Gua; 7,8-benzoflavone (7,8-BF or alpha-naphthoflavone), an inhibitor of CYP1A1 activity a

17 induce preB cell apoptosis in 12 to 24 h; 2) alpha-naphthoflavone, an AhR and cytochrome P-450 inhibi

18 In fact, alpha-naphthoflavone, an AhR antagonist, blocked tobacco

19 ly reduced (2 +/- 1-fold) in the presence of alpha-naphthoflavone, an aryl hydrocarbon receptor (AhR)

20 aryl hydrocarbon receptor (AhR) antagonists alpha-naphthoflavone and 3'-methoxy-4'-nitroflavone (PD1

21 0 altered the responsiveness to the effector alpha-naphthoflavone and the regioselectivity of testost

22 oxy-4-(trifluoromethyl)coumarin (7-BFC), and alpha-naphthoflavone (ANF) as substrates.

23 ray crystallography to 2.7 A resolution with alpha-naphthoflavone (ANF) bound in the active site cavi

24 anthrene (9-AP), 1-pyrenebutanol (1-PB), and alpha-naphthoflavone (ANF) show cooperative spectral bin

25 toluidino)-2-naphthalenesulfonic acid (TNS), alpha-naphthoflavone (ANF), miconazole, and bromocriptin

26 yrenebutanol (1-PB), testosterone (TST), and alpha-naphthoflavone (ANF).

27 ated by the heterotropic allosteric effector alpha-naphthoflavone (ANF).

28 etabolizes, including testosterone (TST) and alpha-naphthoflavone (ANF).

29 alpha-Naphthoflavone binds within an enclosed active sit

30 served over a wide range of progesterone and alpha-naphthoflavone concentrations.

31 human P450 1A2 in complex with the inhibitor alpha-naphthoflavone, determined to a resolution of 1.95

32 alpha-Naphthoflavone had greater receptor affinity (0.79

33 ited NMuMG migration, whereas the antagonist alpha-naphthoflavone induced migration as did AhR knockd

34 avone, determined to a resolution of 1.95 A. alpha-Naphthoflavone is bound in the active site above t

35 alpha-Naphthoflavone-like and 5-hydroxyflavone derivativ

36 i.e. 2,3,7,8-tetrachlorodibenzo-p-dioxin and alpha-naphthoflavone) neither induced apoptosis nor modu

37 distinct ligand sites, with testosterone and alpha-naphthoflavone occupying distinct sites.

38 The AhR antagonist alpha-naphthoflavone prevented B[a]P-induced growth arre

39 In contrast, alpha-naphthoflavone stimulated P450 3A4 by selectively

40 ponsive, respectively, than the wild-type to alpha-naphthoflavone stimulation.

41 211 by Ala also decreased the stimulation by alpha-naphthoflavone, whereas mutations at residues 212-

42 e the interaction of the prototype flavonoid alpha-naphthoflavone with human cytochrome P450s 1A1 and

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