ライフサイエンスコーパス: U46619

1 enosine 5'-diphosphate, A23187, thrombin, or U46619).

2 PH) was induced using a thromboxane agonist (U46619).

3 n response to the thromboxane A(2) analogue (U46619).

4 aggregation induced by thromboxane mimetic, U46619.

5 either high [K+] or the thromboxane analogue U46619.

6 tion in response to receptor activation with U46619.

7 uM ADP and 10 muM of the thromboxane analog, U46619.

8 e intact coronary artery responses to 5-HT + U46619.

9 ivating factor, or the thromboxane A2 analog U46619.

10 endence, reaching a plateau at around 100 nM U46619.

11 ating the responses of MC to the TX analogue U46619.

12 ctivating peptide, low doses of thrombin, or U46619.

13 ly Galpha(12/13)-mediated thromboxane analog U46619.

14 in the absence and presence of the agonist, U46619.

15 tructure in the TP than that of the agonist, U46619.

16 ed in vitro in response to acetylcholine and U46619.

17 considerably better than that of the unbound U46619.

18 termine the contacts between the peptide and U46619.

19 he absence of substrate analogues U44069 and U46619.

20 interact with the enzyme substrate analogue, U46619.

21 serotonin, but not to potassium chloride or U46619.

22 an intact artery after a single addition of U46619.

23 ocytes contract in response to hypoxia or to U46619.

24 shed HPV without attenuating the response to U46619.

25 onary arteries stimulated with either KCl or U46619.

26 ion was induced with the thromboxane mimetic U46619 (0.1-0.4 microg/kg/min).

27 porcine lungs after the thromboxane analogue U46619 (10 pmol.L-1.min-1) increased the mean PVRI from

28 coronary arteries to cumulative addition of U46619 (10(-10) to 10(-5) mol/L), a thromboxane mimetic,

29 coronary arterial rings preconstricted with U46619, 14,15-EET, 11,12-EET, 8,9-EET, and 5,6-EET induc

30 and L-nitroarginine and preconstricted with U46619, 14,15-EEZE (3 micromol/L) inhibited bradykinin (

31 g application of the IP3-generating agonists U46619 (a thromboxane A2 analogue) and ADP.

32 U46619, a PGH2/TxA2 mimetic, induced specific phosphoryl

33 BMS182874 shifts the dose response curve for U46619, a prostaglandin H2 analogue, to the right.

34 n of 100 nmol/L, whereas the effect of TXA2 (U46619, a stable TXA2 mimetic) on inducing proliferation

35 on was induced by the continuous infusion of U46619, a thromboxane A2 analog.

36 U46619, a thromboxane A2 mimetic, but not ADP, caused ac

37 n was produced by the continuous infusion of U46619, a thromboxane A2 mimetic.

38 6) M) to rings preconstricted by 10(-6) M of U46619, a thromboxane receptor agonist, either in the pr

39 ation of mouse platelets by thrombin but not U46619, a thromboxane receptor agonist.

40 Treatment of PC-3 cells by U46619, a TP agonist, induced PC-3 cell contraction, whi

41 eta1 gene ablation reduced the EC(50) of the U46619 agonist in mediating aortic contraction from 18 +

42 Thrombin, histamine, and U46619 all enhanced EGF-stimulated [3H]-thymidine incorp

43 , 11-epoxymethanoprosta-5Z,13E-dienoic acid (U46619), also causes platelet aggregation by concomitant

44 at high concentrations (> 0.2 U/mL), whereas U46619 and ADP alone were ineffective.

45 ut mice had similar contractile responses to U46619 and hypoxia and similar dilation responses to ace

46 the NMR structure of the PGIS-bound form of U46619 and the PGIS crystal structure.

47 cked by a thromboxane receptor (TP) agonist (U46619) and blocked by a TP antagonist (SQ29548), indica

48 arachidonic acid, thromboxane A(2) mimetics (U46619), and very low doses of thrombin and convulxin.

49 ere exposed to pairwise combinations of ADP, U46619, and convulxin to activate the P2Y(1)/P2Y(12), TP

50 otensin II and the thromboxane A(2) mimetic, U46619, and had no significant action on phenylephrine-i

51 phenylephrine, angiotensin II, endothelin-1, U46619, and K(+)-induced membrane depolarization in the

52 hrine, Thrombin receptor activating-peptide, U46619, and ristocetin in samples from (1) healthy volun

53 osphate (ADP)-, 2-methylthioADP (2-MeSADP)-, U46619-, and low-dose thrombin-mediated platelet aggrega

54 tivity to combined stimulation with 5-HT and U46619, as determined by the amplitude and especially th

55 1, H2C, and H20 of U46619 were observed upon U46619 binding to the engineered PGIS in a concentration

56 The U46619-bound enzyme is detected as a 6c/ls heme too, whi

57 responses of six other cardiac afferents to U46619 by 38%.

58 TP activation by the thromboxane A(2) analog U46619 caused inhibition of MaxiKalpha macroscopic condu

59 ypoxic alkalotic lungs, and both hypoxia and U46619 caused significant vasoconstriction in normoxic a

60 In contrast to the FN response to U46619, cGMP and SNAP did not affect the stimulation of

61 ion, where the triangle shape of the unbound U46619 changed to a more compact conformation with an ov

62 PRP) treated with the thromboxane A2 mimetic U46619, collagen and thrombin in presence/absence of var

63 hibited the maximal contractile responses to U46619 compared with arteries from untreated castrated a

64 o norepinephrine and the thromboxane mimetic U46619 compared with young offspring of high-fat-fed nor

65 % and 52 +/- 4% relaxation, respectively, of U46619-contracted rings, whereas 8,9-EET and 5,6-EET did

66 Supplementing a TXA2 analog, U46619, corrected the defect of LIMK1(-/-) platelets in

67 cells expressing the variant D304N TxA(2)R, U46619 did not increase cytosolic free Ca(2+) concentrat

68 , epinephrine and the thromboxane A2 analog, U46619, did not.

69 IC) injections of serotonin, thromboxane A2 (U46619), endothelin 1 or angiotensin II in concentration

70 The bound conformation of U46619 fits the crystal structure of the PGIS substrate

71 PKC and PKD, whereas the thromboxane mimetic U46619 gives rise to transient activation of PKC and PKD

72 s of six agonists (ADP, convulxin, thrombin, U46619, iloprost and GSNO used at 0.1, 1, and 10xEC50; 1

73 ited platelet aggregation induced by ADP and U46619 in a dose-dependent manner.

74 ed increase of cAMP (which is antagonized by U46619 in an ADP-dependent manner) was restored by RPAI-

75 ive responses to the combination of 5-HT and U46619 in untreated VMC were significantly and dose-depe

76 -methanoepoxy-prosta-5Z,13E-dien-1-oic acid (U46619), in contrast, exhibits no preference.

77 -9 alpha,11 alpha-methanoepoxy PGF(2 alpha) (U46619)] in CHO cells transfected with the human TP-P an

78 ditions induced by the thromboxane A2 mimic, U46619, in the pulmonary vascular bed of the cat.

79 It was found that U46619 induced a significant decrease in Galphaq and Gal

80 B (75+/-6%, P<.05 versus control, percent of U46619 induced precontraction) and profoundly hypothermi

81 , and Thr(855) in rat caudal artery, whereas U46619 induced Thr(697) and Thr(855) phosphorylation and

82 ADP, thrombin, or U46619-induced Ca(2+)-independent platelet shape change

83 7632, a Rho kinase (ROCK) inhibitor, blocked U46619-induced cell contraction.

84 ominant-negative mutant of RhoA also blocked U46619-induced cell contraction.

85 neumoniae induced decreases in both KCl- and u46619-induced contractile responses at both time points

86 U46619-induced fibrinogen binding was unchanged after me

87 h the TxA2 agonist U46619 reduced subsequent U46619-induced increases in inositol trisphosphate gener

88 y actions of NO and cGMP at, or proximal to, U46619-induced increases in TGF beta in the suppression

89 AC) receptor selective antagonist, abolished U46619-induced inhibition of adenylyl cyclase.

90 Furthermore, U46619-induced intracellular calcium mobilization and sh

91 Ro 31-8220 had no effect on U46619-induced intracellular calcium mobilization or pla

92 h each protein independently, and diminishes U46619-induced MaxiK channel trans-inhibition as well as

93 ng TP role (with antagonist SQ29,548) in the U46619-induced MaxiK inhibition in human coronaries.

94 Furthermore, inhibition of U46619-induced platelet aggregation by Ro 31-8220 was re

95 change; (ii) ADP restored the inhibition of U46619-induced platelet aggregation by RPAI-1, (iii) PGE

96 functional studies, isoproterenol inhibited U46619-induced platelet aggregation in a concentration-d

97 The standardized meal enhanced U46619-induced platelet P-selectin expression by 23% aft

98 During U46619-induced pulmonary hypertension, INO decreased PAP

99 rmore, pretreatment with forskolin prevented U46619-induced Thr phosphorylations.

100 ein kinase C inhibitor, completely inhibited U46619-induced, but not ADP- or thrombin-induced, platel

101 novel finding that the stable TXA2 analogue, U46619, induces two waves of platelet secretion, each of

102 U46619 infusion produced significant pulmonary vasoconst

103 he responses of six afferents to 5 microg of U46619 injected into the left atrium and attenuated the

104 2.5, 5 and 10 microg of the TxA(2) mimetic, U46619, injected into the left atrium (LA), stimulated s

105 tonin and the stable thromboxane A2 mimetic, U46619, injected through an IC catheter, synergistically

106 r the bicycloendoperoxides U44069, PGH2, and U46619 (Ki = 29-39 nM).

107 mbin and the thromboxane A2 receptor agonist U46619 lead to phosphorylation of Galpha12 and Galpha13.

108 Contractile responses to high molar KCl and u46619 levels and relaxation responses to bradykinin and

109 In addition, AR-C66096 drastically inhibited U46619-mediated platelet aggregation, which was further

110 d consistently to repeated administration of U46619 (n = 6) and to recurrent myocardial ischaemia (n

111 of MaxiK current by thromboxane A2 mimetic, U46619, occurs even when G-protein activity is suppresse

112 ne blue potentiated contractile responses to U46619 of arteries from animals receiving 0.25 and 0.5 m

113 d with stimulation by the thromboxane analog U46619 or ADP.

114 blood exposed to arachidonic acid, collagen, U46619 or protease activated receptor 4 activating pepti

115 ase-activated receptor 4-activating peptide, U46619, or ADP.

116 tured VSMCs to either TPr agonists, IBOP and U46619, or exogenous hydrogen peroxide (H2O2) caused tim

117 antagonist naloxone, the thromboxane mimetic U46619, or the cannabinoid antagonist AM251.

118 rence in the contraction by the TXA2 agonist U46619, or TP receptor expression in arteries from diffe

119 s analogues did not inhibit ADP-, collagen-, U46619-, or SFLLRN-induced platelet activation or the ab

120 oconstriction to the thromboxane A2 mimetic, U46619 (P < 0.05) and sensitivity to potassium (P < 0.01

121 vasoconstrictor responses to norepinephrine, U46619, PGF2alpha, vasopressin, BAY K8644; biphasic resp

122 d hyperpolarization (EDH)-type relaxation in U46619-precontracted rings.

123 -6 position is closer to the C-9 position of U46619 provided the first experimental data for understa

124 A TXA2 agonist, U46619, reconstitutes both migration and angiogenesis re

125 Prior treatment with the TxA2 agonist U46619 reduced subsequent U46619-induced increases in in

126 e shift of the FP(o) versus voltage curve by U46619 relative to the control was less prominent when b

127 a to six different agonists (ADP, convulxin, U46619, SFLLRN, AYPGKF and PGE(2)) at three concentratio

128 In parallel, both IBOP and U46619 significantly increased the production of reactiv

129 it was found that the TXA2 receptor agonist U46619 stimulated [35S]guanosine 5'-O-(3-thiotriphosphat

130 U46619 stimulated phosphoinositide 3-kinase (PI3K)-depen

131 Agonist (ADP, thrombin, or U46619)-stimulated but not resting platelets adhered to

132 -stimulated and thromboxane receptor agonist U46619-stimulated platelet aggregation in a concentratio

133 olished HPV without affecting contraction to U46619, suggesting that ROS act as second messengers.

134 Interestingly, upon addition of the agonist, U46619, the Galphaq-Ct peptide's binding affinity for th

135 The binding of U46619 to the PGIS protein was demonstrated by 1D NMR ti

136 ing of a substrate (prostaglandin H2) mimic (U46619) to the engineered prostacyclin (PGI2) synthase (

137 agonists such as ADP, thromboxane analogue (U46619), TRAP, or convulxin.

138 e aortic endothelial cells to either IBOP or U46619, two structurally related thromboxane A(2) mimeti

139 ditions induced by the thromboxane A2 mimic, U46619 (Upjohn, Kalamazoo, MI).

140 he conformational changes of the peptide and U46619 using the comparison of the cross-peaks between t

141 ood vessel contractility, as the response to U46619 was attenuated in isolated perfused hind limbs fr

142 between the constrained F/G loop peptide and U46619 was confirmed by the observation of the conformat

143 However, subsequent reactivity to U46619 was enhanced in hypoxic alkalotic lungs, and both

144 response was abolished while the response to U46619 was maintained in mutant (rho(0)) PA myocytes lac

145 Vasoconstriction to the TP agonist, U46619 was reduced by Rho kinase inhibition.

146 rioles to the vasoconstriction-inducing drug U46619 was reduced.

147 he response to the thromboxane A(2) analogue U46619 was unaffected.

148 radioactive representative from this group, U46619, was not transported.

149 Responses to hypoxia and U46619 were also compared after 60-80 mins of hypocarbic

150 al change and 3D structure of the PGIS-bound U46619 were further demonstrated by 2D 1H NMR experiment

151 reas pressor responses to norepinephrine and U46619 were not changed.

152 l shifts of protons at C-11, H2C, and H20 of U46619 were observed upon U46619 binding to the engineer

153 loop segment in the presence and absence of U46619 were obtained, and these data were used to predic

154 thromboxane A(2) receptor (TxA(2)R) agonist U46619 were reduced in P1 compared with controls, wherea

155 Pulmonary artery dose responses to U46619 were then measured in control lungs.

156 ADP and U46619 were without effect.

157 duced by the thromboxane A2 receptor agonist U46619, which suggest a NO-independent vasodilatador eff

158 the cross-peaks between the NOESY spectra of U46619 with the peptide, without the peptide, and the pe

159 egation formation and secretion triggered by U46619, without affecting Ca(2+) increase and shape chan