ライフサイエンスコーパス: butaprost

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1 as confirmed using the EP2-selective agonist butaprost.

2 ed the inhibitory effects of both PGE(2) and butaprost.

3 lprostone, but not the EP2 receptor agonist, butaprost.

4 EP1R antagonist SC-19220 or the EP2R agonist butaprost.

5 nd IgG class switching, exogenous PGE(2) and butaprost, a selective EP2 agonist, augmented AID mRNA/p

6 e the PGE(2)-dependent pathway, we show that butaprost, a specific EP2 agonist, stimulates progestero

7 Butaprost also induced the activation of Akt, ERK1/2, an

8 Butaprost also mimicked the effect of OxPAPC on the regu

9 clic AMP ([cAMP]i) by PGE2, misoprostol, and butaprost and of increases in the intracellular concentr

10 Butaprost and ONO-AE1-329, EP(2) and EP(4) receptor agon

11 The application of butaprost and sulprostone triggered neuropeptide exocyto

12 he effects of specific EP2 and EP3 agonists (butaprost and sulprostone) in cultured trigeminal gangli

13 Agonists of E prostanoid receptors EP2 (butaprost) and EP1/3 (sulprostone) mimicked PGE2, while

14 EP2 prostaglandin receptor activation with butaprost blocks the TGFbeta1-stimulated expression of C

15 and misoprostol, and EP2 R-selective agonist butaprost but not the EP1 R-selective antagonist SC-1922

16 fects were mimicked fully by the EP2 agonist butaprost but only weakly by the EP1/EP3 agonist 17-phen

17 The selective EP2 agonist butaprost, but neither the EP1/EP3 agonist sulprostone n

18 Treatment with PGE2 or EP2 selective agonist butaprost, but not EP4 agonist CAY10598, increased cAMP

19 icked by the EP2-selective receptor agonist, butaprost, by cAMP activation, and were lost in murine l

20 ngle topical application of the EP2 agonist, butaprost, dose-dependently increased keratinocyte repli

21 nophosphate acetoxymethyl ester mimicked all butaprost effects.

22 n F2alpha (PGF2alpha) (FP receptor agonist), Butaprost (EP2 receptor agonist), and Bimatoprost (a pro

23 stol), EP2 -selective (ONO-AE1-259, AH13205, butaprost-free acid) and EP4 -selective (L-902,688, TCS2

24 However, an EP2 agonist (butaprost) has no effect on MMP-9 expression, and macrop

25 to beta-arrestin1-dependent EGFR activation, butaprost increased PKA activation, as measured by phosp

26 Butaprost induced beta-arrestin1-Src complex formation a

27 In resting microglia, butaprost induced cAMP formation and altered the mRNA ex

28 monophosphorothioate (R(P)-cAMPS)) decreased butaprost-induced cAMP-response element-binding protein

29 decreased EGFR activation but did not affect butaprost-induced PKA activation, thus indicating that t

30 at the mRNA for the murine EP4 receptor, the butaprost-insensitive PGE2 receptor that couples to Gs,

31 d little effect on membrane current, whereas butaprost methyl ester (an EP2 agonist) mimicked the eff

32 tors, direct addition of sulprostone but not butaprost mimicked PGE2, suggesting that PGE2 engaged EP

33 In contrast, the EP2 receptor agonist butaprost, not the E1/E3 receptor agonist sulprostone, s

34 y finding that PGE2 and misoprostol, but not butaprost or sulprostone, evoked increases in the intrac

35 (2) production, and PGE(2), the EP2 agonist (butaprost) or EP4 agonist (PGE(1) alcohol), was applied.

36 ministration of either EP2-specific agonist, butaprost, or 8-Br-cAMP, a cell-permeable cAMP analog, p

37 the TGFbeta1-stimulated CCN2/CTGF by PGE(2), butaprost, or forskolin is due to p38, ERK, and JNK MAP

38 stone triggered neuropeptide exocytosis, and butaprost sensitized capsaicin responses.

39 not with 10(-6) M PGF2alpha, PGD2, PGI2, or butaprost, suggesting a principal dependence on EP3 Rs.

40 addition of PGE2 or the EP2 receptor agonist butaprost to PMK produced a dose- and time-dependent dec

41 dent inhibition of Ca(2+) signals by PGE2 or butaprost (to activate EP2 receptors selectively), but i

42 The EP2 specific agonist butaprost was shown to mimic the effect of OxPAPC on the

43 1%) VSMCs, whereas the EP2 receptor agonist, butaprost, was without effect.

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