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1 PH) was induced using a thromboxane agonist (U46619).
2 dent of contractile stimulus (oxytocin, KCl, U46619).
3 enosine 5'-diphosphate, A23187, thrombin, or U46619).
4 n response to the thromboxane A(2) analogue (U46619).
5 ocytes contract in response to hypoxia or to U46619.
6 shed HPV without attenuating the response to U46619.
7 onary arteries stimulated with either KCl or U46619.
8  aggregation induced by thromboxane mimetic, U46619.
9 either high [K+] or the thromboxane analogue U46619.
10 tion in response to receptor activation with U46619.
11 e intact coronary artery responses to 5-HT + U46619.
12 ivating factor, or the thromboxane A2 analog U46619.
13 endence, reaching a plateau at around 100 nM U46619.
14 ating the responses of MC to the TX analogue U46619.
15 uM ADP and 10 muM of the thromboxane analog, U46619.
16 ctivating peptide, low doses of thrombin, or U46619.
17 ly Galpha(12/13)-mediated thromboxane analog U46619.
18  in the absence and presence of the agonist, U46619.
19 tructure in the TP than that of the agonist, U46619.
20 ed in vitro in response to acetylcholine and U46619.
21 considerably better than that of the unbound U46619.
22  by collagen and the thromboxane A(2) analog U46619.
23 termine the contacts between the peptide and U46619.
24 he absence of substrate analogues U44069 and U46619.
25 interact with the enzyme substrate analogue, U46619.
26  serotonin, but not to potassium chloride or U46619.
27  an intact artery after a single addition of U46619.
28 ion was induced with the thromboxane mimetic U46619 (0.1-0.4 microg/kg/min).
29 porcine lungs after the thromboxane analogue U46619 (10 pmol.L-1.min-1) increased the mean PVRI from
30  coronary arteries to cumulative addition of U46619 (10(-10) to 10(-5) mol/L), a thromboxane mimetic,
31  coronary arterial rings preconstricted with U46619, 14,15-EET, 11,12-EET, 8,9-EET, and 5,6-EET induc
32  and L-nitroarginine and preconstricted with U46619, 14,15-EEZE (3 micromol/L) inhibited bradykinin (
33 g application of the IP3-generating agonists U46619 (a thromboxane A2 analogue) and ADP.
34                                              U46619, a PGH2/TxA2 mimetic, induced specific phosphoryl
35 BMS182874 shifts the dose response curve for U46619, a prostaglandin H2 analogue, to the right.
36 zation from -90 to +60 mV in the presence of U46619, a stable analog of prostaglandin H(2) Half-maxim
37 n of 100 nmol/L, whereas the effect of TXA2 (U46619, a stable TXA2 mimetic) on inducing proliferation
38 on was induced by the continuous infusion of U46619, a thromboxane A2 analog.
39                                              U46619, a thromboxane A2 mimetic, but not ADP, caused ac
40 n was produced by the continuous infusion of U46619, a thromboxane A2 mimetic.
41 6) M) to rings preconstricted by 10(-6) M of U46619, a thromboxane receptor agonist, either in the pr
42 ation of mouse platelets by thrombin but not U46619, a thromboxane receptor agonist.
43                   Treatment of PC-3 cells by U46619, a TP agonist, induced PC-3 cell contraction, whi
44 eta1 gene ablation reduced the EC(50) of the U46619 agonist in mediating aortic contraction from 18 +
45                     Thrombin, histamine, and U46619 all enhanced EGF-stimulated [3H]-thymidine incorp
46 , 11-epoxymethanoprosta-5Z,13E-dienoic acid (U46619), also causes platelet aggregation by concomitant
47 at high concentrations (> 0.2 U/mL), whereas U46619 and ADP alone were ineffective.
48 re stimulated with or without the TP agonist U46619 and assayed for prostanoid production.
49 metry, we also demonstrate direct binding of U46619 and cysteinyl leukotrienes C(4), D(4) and E(4) to
50 ut mice had similar contractile responses to U46619 and hypoxia and similar dilation responses to ace
51 ause prostaglandin F receptor activated with U46619 and prostaglandin E(2) receptor subtype 3 activat
52  the NMR structure of the PGIS-bound form of U46619 and the PGIS crystal structure.
53 cked by a thromboxane receptor (TP) agonist (U46619) and blocked by a TP antagonist (SQ29548), indica
54 arachidonic acid, thromboxane A(2) mimetics (U46619), and very low doses of thrombin and convulxin.
55 ere exposed to pairwise combinations of ADP, U46619, and convulxin to activate the P2Y(1)/P2Y(12), TP
56 otensin II and the thromboxane A(2) mimetic, U46619, and had no significant action on phenylephrine-i
57 phenylephrine, angiotensin II, endothelin-1, U46619, and K(+)-induced membrane depolarization in the
58 s to endothelin-1 (ET-1), thromboxane analog U46619, and norepinephrine were mediated by ET(A), throm
59 hrine, Thrombin receptor activating-peptide, U46619, and ristocetin in samples from (1) healthy volun
60 mbinant PDI and higher inhibitory effects on U46619- and/or collagen-induced platelet aggregation tha
61 osphate (ADP)-, 2-methylthioADP (2-MeSADP)-, U46619-, and low-dose thrombin-mediated platelet aggrega
62 tivity to combined stimulation with 5-HT and U46619, as determined by the amplitude and especially th
63 1, H2C, and H20 of U46619 were observed upon U46619 binding to the engineered PGIS in a concentration
64                                          The U46619-bound enzyme is detected as a 6c/ls heme too, whi
65  responses of six other cardiac afferents to U46619 by 38%.
66 TP activation by the thromboxane A(2) analog U46619 caused inhibition of MaxiKalpha macroscopic condu
67 ypoxic alkalotic lungs, and both hypoxia and U46619 caused significant vasoconstriction in normoxic a
68            In contrast to the FN response to U46619, cGMP and SNAP did not affect the stimulation of
69 ion, where the triangle shape of the unbound U46619 changed to a more compact conformation with an ov
70 PRP) treated with the thromboxane A2 mimetic U46619, collagen and thrombin in presence/absence of var
71 hibited the maximal contractile responses to U46619 compared with arteries from untreated castrated a
72 o norepinephrine and the thromboxane mimetic U46619 compared with young offspring of high-fat-fed nor
73 % and 52 +/- 4% relaxation, respectively, of U46619-contracted rings, whereas 8,9-EET and 5,6-EET did
74                 Supplementing a TXA2 analog, U46619, corrected the defect of LIMK1(-/-) platelets in
75  cells expressing the variant D304N TxA(2)R, U46619 did not increase cytosolic free Ca(2+) concentrat
76 , epinephrine and the thromboxane A2 analog, U46619, did not.
77 IC) injections of serotonin, thromboxane A2 (U46619), endothelin 1 or angiotensin II in concentration
78                    The bound conformation of U46619 fits the crystal structure of the PGIS substrate
79 PKC and PKD, whereas the thromboxane mimetic U46619 gives rise to transient activation of PKC and PKD
80 s of six agonists (ADP, convulxin, thrombin, U46619, iloprost and GSNO used at 0.1, 1, and 10xEC50; 1
81 ited platelet aggregation induced by ADP and U46619 in a dose-dependent manner.
82 the absence of the vessel constricting agent U46619 in acute slices, SMCs and EPs revealed only spars
83 ed increase of cAMP (which is antagonized by U46619 in an ADP-dependent manner) was restored by RPAI-
84 nstriction caused by the thromboxane mimetic U46619 in mesenteric resistance arteries of wild-type an
85 ilatation in arteries constricted with 1 mum U46619 in the presence of 140 mum suramin and 1 mum praz
86 ive responses to the combination of 5-HT and U46619 in untreated VMC were significantly and dose-depe
87 -methanoepoxy-prosta-5Z,13E-dien-1-oic acid (U46619), in contrast, exhibits no preference.
88 -9 alpha,11 alpha-methanoepoxy PGF(2 alpha) (U46619)] in CHO cells transfected with the human TP-P an
89 ditions induced by the thromboxane A2 mimic, U46619, in the pulmonary vascular bed of the cat.
90                            It was found that U46619 induced a significant decrease in Galphaq and Gal
91 B (75+/-6%, P<.05 versus control, percent of U46619 induced precontraction) and profoundly hypothermi
92 , and Thr(855) in rat caudal artery, whereas U46619 induced Thr(697) and Thr(855) phosphorylation and
93                            ADP, thrombin, or U46619-induced Ca(2+)-independent platelet shape change
94 7632, a Rho kinase (ROCK) inhibitor, blocked U46619-induced cell contraction.
95 ominant-negative mutant of RhoA also blocked U46619-induced cell contraction.
96 neumoniae induced decreases in both KCl- and u46619-induced contractile responses at both time points
97                                              U46619-induced fibrinogen binding was unchanged after me
98 h the TxA2 agonist U46619 reduced subsequent U46619-induced increases in inositol trisphosphate gener
99 y actions of NO and cGMP at, or proximal to, U46619-induced increases in TGF beta in the suppression
100 AC) receptor selective antagonist, abolished U46619-induced inhibition of adenylyl cyclase.
101                                 Furthermore, U46619-induced intracellular calcium mobilization and sh
102                  Ro 31-8220 had no effect on U46619-induced intracellular calcium mobilization or pla
103 h each protein independently, and diminishes U46619-induced MaxiK channel trans-inhibition as well as
104 ng TP role (with antagonist SQ29,548) in the U46619-induced MaxiK inhibition in human coronaries.
105                   Furthermore, inhibition of U46619-induced platelet aggregation by Ro 31-8220 was re
106  change; (ii) ADP restored the inhibition of U46619-induced platelet aggregation by RPAI-1, (iii) PGE
107  functional studies, isoproterenol inhibited U46619-induced platelet aggregation in a concentration-d
108               The standardized meal enhanced U46619-induced platelet P-selectin expression by 23% aft
109                                       During U46619-induced pulmonary hypertension, INO decreased PAP
110 rmore, pretreatment with forskolin prevented U46619-induced Thr phosphorylations.
111 boys with hypospadias demonstrated increased U46619-induced vasoconstriction (P = 0.009) and reduced
112 ein kinase C inhibitor, completely inhibited U46619-induced, but not ADP- or thrombin-induced, platel
113 novel finding that the stable TXA2 analogue, U46619, induces two waves of platelet secretion, each of
114                                              U46619 infusion produced significant pulmonary vasoconst
115 he responses of six afferents to 5 microg of U46619 injected into the left atrium and attenuated the
116  2.5, 5 and 10 microg of the TxA(2) mimetic, U46619, injected into the left atrium (LA), stimulated s
117 tonin and the stable thromboxane A2 mimetic, U46619, injected through an IC catheter, synergistically
118 r the bicycloendoperoxides U44069, PGH2, and U46619 (Ki = 29-39 nM).
119 mbin and the thromboxane A2 receptor agonist U46619 lead to phosphorylation of Galpha12 and Galpha13.
120  Contractile responses to high molar KCl and u46619 levels and relaxation responses to bradykinin and
121 In addition, AR-C66096 drastically inhibited U46619-mediated platelet aggregation, which was further
122 d consistently to repeated administration of U46619 (n = 6) and to recurrent myocardial ischaemia (n
123  of MaxiK current by thromboxane A2 mimetic, U46619, occurs even when G-protein activity is suppresse
124 ne blue potentiated contractile responses to U46619 of arteries from animals receiving 0.25 and 0.5 m
125 d with stimulation by the thromboxane analog U46619 or ADP.
126 blood exposed to arachidonic acid, collagen, U46619 or protease activated receptor 4 activating pepti
127 ase-activated receptor 4-activating peptide, U46619, or ADP.
128 tured VSMCs to either TPr agonists, IBOP and U46619, or exogenous hydrogen peroxide (H2O2) caused tim
129 antagonist naloxone, the thromboxane mimetic U46619, or the cannabinoid antagonist AM251.
130 rence in the contraction by the TXA2 agonist U46619, or TP receptor expression in arteries from diffe
131 s analogues did not inhibit ADP-, collagen-, U46619-, or SFLLRN-induced platelet activation or the ab
132 oconstriction to the thromboxane A2 mimetic, U46619 (P < 0.05) and sensitivity to potassium (P < 0.01
133 vasoconstrictor responses to norepinephrine, U46619, PGF2alpha, vasopressin, BAY K8644; biphasic resp
134 d hyperpolarization (EDH)-type relaxation in U46619-precontracted rings.
135 -6 position is closer to the C-9 position of U46619 provided the first experimental data for understa
136                              A TXA2 agonist, U46619, reconstitutes both migration and angiogenesis re
137        Prior treatment with the TxA2 agonist U46619 reduced subsequent U46619-induced increases in in
138 e shift of the FP(o) versus voltage curve by U46619 relative to the control was less prominent when b
139 a to six different agonists (ADP, convulxin, U46619, SFLLRN, AYPGKF and PGE(2)) at three concentratio
140                   In parallel, both IBOP and U46619 significantly increased the production of reactiv
141  it was found that the TXA2 receptor agonist U46619 stimulated [35S]guanosine 5'-O-(3-thiotriphosphat
142                                              U46619 stimulated phosphoinositide 3-kinase (PI3K)-depen
143                   Agonist (ADP, thrombin, or U46619)-stimulated but not resting platelets adhered to
144 -stimulated and thromboxane receptor agonist U46619-stimulated platelet aggregation in a concentratio
145 olished HPV without affecting contraction to U46619, suggesting that ROS act as second messengers.
146 Interestingly, upon addition of the agonist, U46619, the Galphaq-Ct peptide's binding affinity for th
147                               The binding of U46619 to the PGIS protein was demonstrated by 1D NMR ti
148 ing of a substrate (prostaglandin H2) mimic (U46619) to the engineered prostacyclin (PGI2) synthase (
149  agonists such as ADP, thromboxane analogue (U46619), TRAP, or convulxin.
150 e aortic endothelial cells to either IBOP or U46619, two structurally related thromboxane A(2) mimeti
151 ditions induced by the thromboxane A2 mimic, U46619 (Upjohn, Kalamazoo, MI).
152 he conformational changes of the peptide and U46619 using the comparison of the cross-peaks between t
153 ood vessel contractility, as the response to U46619 was attenuated in isolated perfused hind limbs fr
154 between the constrained F/G loop peptide and U46619 was confirmed by the observation of the conformat
155            However, subsequent reactivity to U46619 was enhanced in hypoxic alkalotic lungs, and both
156 response was abolished while the response to U46619 was maintained in mutant (rho(0)) PA myocytes lac
157          Vasoconstriction to the TP agonist, U46619 was reduced by Rho kinase inhibition.
158 rioles to the vasoconstriction-inducing drug U46619 was reduced.
159 he response to the thromboxane A(2) analogue U46619 was unaffected.
160  radioactive representative from this group, U46619, was not transported.
161                     Responses to hypoxia and U46619 were also compared after 60-80 mins of hypocarbic
162 al change and 3D structure of the PGIS-bound U46619 were further demonstrated by 2D 1H NMR experiment
163 reas pressor responses to norepinephrine and U46619 were not changed.
164 l shifts of protons at C-11, H2C, and H20 of U46619 were observed upon U46619 binding to the engineer
165  loop segment in the presence and absence of U46619 were obtained, and these data were used to predic
166  thromboxane A(2) receptor (TxA(2)R) agonist U46619 were reduced in P1 compared with controls, wherea
167           Pulmonary artery dose responses to U46619 were then measured in control lungs.
168                                      ADP and U46619 were without effect.
169 duced by the thromboxane A2 receptor agonist U46619, which suggest a NO-independent vasodilatador eff
170 d responses of several structural analogs of U46619 with modifications to a similar extent all around
171 the cross-peaks between the NOESY spectra of U46619 with the peptide, without the peptide, and the pe
172 egation formation and secretion triggered by U46619, without affecting Ca(2+) increase and shape chan

 
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