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1 h is mediated, in part, by activation of the thromboxane receptor.
2 +) ionophore or by agonists for thrombin and thromboxane receptors.
3 s as a signaling protein in association with thromboxane receptors.
4 ation of Sp1 contributes to up-regulation of thromboxane receptors.
5 gonists, they are unlikely to be mediated by thromboxane receptors.
6            The voltage-induced modulation of thromboxane receptor activity was observed on the level
7 ed human platelet aggregation induced by the thromboxane receptor agonist U46,619, and this effect wa
8  selectively blocked both ADP-stimulated and thromboxane receptor agonist U46619-stimulated platelet
9 ings preconstricted by 10(-6) M of U46619, a thromboxane receptor agonist, either in the presence or
10                       Liraglutide attenuated thromboxane receptor agonist-induced activation as measu
11  pretreatment with liraglutide or vehicle on thromboxane receptor agonist-induced in vitro activation
12 ouse platelets by thrombin but not U46619, a thromboxane receptor agonist.
13 at seven positions throughout the human K562 thromboxane receptor and analyzed mutant receptor radiol
14 d two contribute to proper ligand binding to thromboxane receptors and show the importance of discret
15 c acid (14) with Kd = 9.9 +/- 0.4 nM for the thromboxane receptor antagonism and IC50 = 55.0 +/- 17.9
16 amine, antioxidant treatment with Tempol and thromboxane receptor antagonism with SQ-29548) were show
17     The thromboxane inhibitors tested were a thromboxane receptor antagonist (TXRA) and a thromboxane
18  leukotriene synthesis inhibitor, n = 5; and thromboxane receptor antagonist, n = 6).
19 oxygenase inhibitor, or SQ29548, a selective thromboxane receptor antagonist.
20 ation of WT platelets that was reversed by a thromboxane receptor antagonist.
21 lass of dual cyclooxygenase (COX) inhibitors/thromboxane receptor antagonists (COXTRANs) based on the
22 ese effects are prevented by pharmacological thromboxane receptor antagonists, they are unlikely to b
23 tease-activated receptor-1) antagonists, and thromboxane receptor antagonists.
24 tion was abolished by combined histamine and thromboxane receptor antagonists.
25  and prostaglandin E(2) receptors as well as thromboxane receptors are activated upon depolarization,
26  (positions 68 and 257) had little effect on thromboxane receptor binding or signaling.
27 (position 183) extracellular loop eliminated thromboxane receptor binding, consistent with the existe
28                                              Thromboxane receptor blockade lowered TNF and leukotrien
29 with little further antagonism by additional thromboxane receptor blockade.
30 nce rates also occurred in the presence of a thromboxane receptor blocker (n = 4), even when blood le
31          Chronic nitric oxide synthase I and thromboxane receptor deficiency did not change TGF respo
32 racellular loop, especially cysteine 223, in thromboxane receptor-effector coupling.
33 ggest that modulation of Sp1 levels controls thromboxane receptor expression during megakaryocytic di
34 aracterized the promoter region of the human thromboxane receptor gene and localized PMA-responsive e
35                                 Heterologous thromboxane receptor gene promoter/thymidilate kinase re
36 tion, oxidation, or sulfhydryl alkylation on thromboxane receptors have suggested a role for cysteine
37                       Expression of platelet thromboxane receptors is transcriptionally increased dur
38 pi PGF2alpha does not activate either of the thromboxane receptor isoforms described in platelets.
39 or and caused only minimal activation of the thromboxane receptor isoforms stably expressed in HEK 29
40  response directly, via either of the cloned thromboxane receptor isoforms stably expressed in human
41 pe were found in nitric oxide synthase I and thromboxane receptor knockout mice.
42 the rank order of affinities for a series of thromboxane receptor ligands to bind to cloned human TPa
43 ipase A2, cyclooxygenase, or blockade of the thromboxane receptor markedly reduced the effects of H2S
44 ncreased Sp1 mRNA levels prior to increasing thromboxane receptor mRNA, suggesting that up-regulation
45 n potential.(1) Their studies reveal a novel thromboxane receptor mutation (TP-V241G) in humans that
46 EP2/DP on preosteoclasts and subtype EP1 and thromboxane receptors on stromal/osteoblast cells.
47                            Inhibition of the thromboxane receptor or cyclooxygenase-2 dramatically at
48 sed placental or endothelial isoforms of the thromboxane receptor or for binding of thromboxane ligan
49 cement by activating PGF(2alpha) receptor or thromboxane receptor, or approximately 15% enhancement b
50 nocytes and macrophages depends on autocrine thromboxane receptor signaling and that under normal con
51 d LDL-mediated PGIS nitration and associated thromboxane receptor stimulation might be important in t
52 iscovered a robust voltage dependence of the thromboxane receptor (TP receptor) on the receptor level
53  effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) agonist (U46619) and blocked b
54                   However, although a single thromboxane receptor (TP) gene has been identified, two
55 is a GTP binding protein that couples to the thromboxane receptor (TP), but also functions as tissue
56 aglandin E(2) receptor subtype 4 (EP(4)) and thromboxane receptor (TP).
57 L receptor-deficient mice) by activating the thromboxane receptor (TP).
58 TXA2 and isoprostanes) which act through the thromboxane receptor (TP).
59 ndertaken to determine the potential role of thromboxane receptors (TP) in bladder cancer.
60 menon by demonstrating that H1 histamine and thromboxane receptors utilize the same mechanism to augm
61 ependent on a non-thromboxane agonist of the thromboxane receptor, whereas vasodilatory mechanisms of