ライフサイエンスコーパス: RU-486

1 abrogated by the PR antagonist mifepristone (RU-486).

2 ine were abrogated by the GRalpha-antagonist RU 486.

3 ed by the glucocorticoid receptor antagonist RU 486.

4 is effect was reversed by the PR antagonist, RU 486.

5 This effect is blocked by the antiprogestin RU 486.

6 the glucocorticoid receptor (GR) antagonist RU 486.

7 involving treatments with corticosterone and RU-486.

8 application of the glucocorticoid antagonist RU-486.

9 activity was inhibited with the addition of RU-486.

10 , with and without the competitive inhibitor RU-486.

11 d by the steroid hormone receptor antagonist RU-486.

12 t of rats with the glucocorticoid antagonist RU-486.

13 tion as that obtained with the antiprogestin RU-486.

14 with the glucocorticoid receptor antagonist RU-486.

15 MAP kinase activity by N-CAM was reversed by RU-486.

16 ly reversed by the glucocorticoid antagonist RU-486.

17 ed by N-CAM was abolished in the presence of RU-486.

18 as suppressed by the progesterone antagonist RU-486.

19 s, which were prevented by co-treatment with RU-486.

20 ronolactone (1-10 microM), the GR antagonist RU-486 (1-10 microM), or the protein synthesis inhibitor

21 icoid receptor (GR) antagonist mifepristone (RU-486; 10(-6) mol/L) blocked the inhibitory effect of D

22 oligos or pharmacological blockade of PRs by RU-486 [11beta-[p-(dimethylamino)phenyl]-17beta-hydroxy-

23 ion can be blocked by the antiglucocorticoid RU-486, 2) dexamethasone-dependent transcriptional activ

24 with the glucocorticoid receptor antagonist RU-486 (20 mg/kg).

25 Inclusion of RU 486 (a glucocorticoid antagonist) with cortisol preve

26 ynthesis, and their induction was blocked by RU-486 (a progesterone receptor antagonist).

27 Treatment of the mice with RU 486, a glucocorticoid receptor antagonist, prior to r

28 Treatment of cells with RU 486, a glucocorticoid receptor blocker, reversed the

29 Treatment of the animals with RU-486, a glucocorticoid receptor antagonist, inhibited

30 RU-486, a potent glucocorticoid antagonist, reversed the

31 i-gp130 Abs or the glucocorticoid antagonist RU-486 abolished this synergistic effect.

32 Since RU 486 acts as an antagonist to progesterone's action at

33 RU 486 alone had no apparent effects on basal [Ca2+]i or

34 effect, although the progesterone antagonist RU 486 also blocked KV and KCa channels.

35 While RU 486 also reversed DEX-induced repression of Ia mRNA e

36 or absence of corticoid-receptor antagonist RU-486 and cannabinoid-receptor agonist WIN55,212-2.

37 stem controlled by the progesterone analogue RU-486 and the other controlled by the tetracycline deri

38 erone receptor (hPR) inhibitor Mifepristone (RU-486) and other hPR ligands, a new class of potential

39 The glucocorticoid antagonist RU 486 blocked both DEX and HS-induced enhancement of IF

40 The antiprogestin RU-486 blocks progestin stimulation of growth, indicatin

41 nding assay, we confirmed that hGRbeta bound RU-486 but not the hGRalpha ligand dexamethasone.

42 In the first experiment we show that RU 486 can antagonize progesterone's inhibitory effect o

43 lcineurin activation, but co-incubation with RU-486 completely blocked enzyme stimulation.

44 In accord with previous findings that RU-486 could partially prevent the proliferative effects

45 ice with the glucocorticoid receptor blocker RU 486 decreased plasma glucose by 50% and reduced PEPCK

46 ber of glucocorticoid antagonists, including RU-486, dehydroepiandrosterone, and progesterone.

47 at occupation of hGRbeta with the antagonist RU-486 diminishes that capacity despite the lack of heli

48 RU-486 displayed a dose-dependent antagonism to drug-ind

49 Furthermore, the glucocorticoid antagonist RU-486 in combination with C. sordellii lethal toxin add

50 ids and glucocorticoid receptor blockade, by RU 486, increases striatal preproenkephalin (PPenk) mRNA

51 ed by the glucocorticoid receptor antagonist RU-486, indicating that these triterpenoids do not act t

52 of DEX-induced RFP-GRalpha were faster than RU-486-induced nuclear shuttling.

53 eries of 57 related compounds indicated that RU-486 is thus far the only identified ligand that inter

54 with the glucocorticoid receptor antagonist RU 486 +/- metyrapone between postnatal days 2 and 4.

55 n, treatment of cells with the GR antagonist RU-486 (Mifepristone) prevented promoter activation by e

56 mRNA expression, as blockade of the GR with RU 486 or ablation of Sp1 binding with mithramycin abrog

57 tu, which was prevented by co-treatment with RU-486 or WIN55,212-2.

58 Moreover, progesterone receptor antagonist RU-486 partially reversed the effects of P4 on NF-kappaB

59 The steroid receptor antagonist RU 486 prevented this proteolytic response.

60 Treatment of WA stressed rats with RU-486 prevented these changes.

61 th the progesterone antagonist mifepristone (RU 486) prevented mammary tumorigenesis.

62 treated with or without dexamethasone (Dex), RU-486, spironolactone, or vehicle.

63 We administered the PR antagonist, RU-486, subcutaneously to male and female rats on postna

64 The steroid-receptor antagonist RU 486 suppressed this response to the addition of dexam

65 n the presence and/or absence of cortisol or RU 486), the results show that cortisol stimulation of g

66 osis quotient (LQ) was observed and neonatal RU-486 treatment did not alter this behavior.

67 In contrast, neonatal RU-486 treatment increased adult male sexual behavior an

68 al abortion with mifepristone (also known as RU-486) used with misoprostol were reported.

69 This effect of RU-486 was confirmed with transiently expressed wild-typ

70 RU-486 was tested for antagonism of MYOC protein express

71 Progesterone receptor antagonist RU-486 were further applied.

72 The selective interaction of RU-486 with hGRbeta was also supported by molecular mode