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1 ibiting nanomolar activity on both COX-2 and TP receptor.
2 owed a similar reaction to depolarization as TP receptor.
3 hromboxane A2 elicits scratching through its TP receptor.
4 ossible ligand-binding sites on native human TP receptor.
5 oltage modulates the general conformation of TP receptor.
6  extra- and the intracellular domains of the TP receptor.
7 zation affected the agonist affinity for the TP receptor.
8  abolished binding affinity at beta 2-AR and TP receptors.
9 macologic blockade and genetic disruption of TP receptors.
10 t responsiveness of wild type but not mutant TP receptors.
11  thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor.
12 A(2) and signaling through the T prostanoid (TP) receptor.
13 he gene encoding the thromboxane-prostanoid (TP) receptor.
14 tic and lung tissue-associated T prostanoid (TP) receptors.
15 elet-adherent granulocytes and T-prostanoid (TP) receptors.
16 by G protein-coupled thromboxane-prostanoid (TP) receptors.
17 s to agonist-specific desensitization of the TP receptor, 2) PKC-induced desensitization of TP recept
18                   Thromboxane A(2) receptor (TP receptor), a prostanoid receptor, belongs to the G pr
19                  The human thromboxane A(2) (TP) receptor, a member of the G protein-coupled receptor
20 ted by cell culture studies that showed that TP receptor activation increased Abeta and secreted APP
21 ne (TP) receptor antagonist, suggesting that TP receptor activation mediates the effects of iPF(2alph
22                                              TP receptor activity doubled upon depolarization from -9
23 finity and significantly lower beta 1-AR and TP receptor affinities.
24 lter beta 2-AR affinity, but greatly reduced TP receptor affinity (380- and 1200-fold, respectively).
25 ta 2-AR and thromboxane A2/prostaglandin H2 (TP) receptor affinity.
26                              Infusion of the TP receptor agonist U-46619 causes transient increases i
27 of 10 microM PGF(2alpha) was mimicked by the TP receptor agonist U-46619.
28                                 However, the TP receptor agonists U-46,619, PGF2alpha, and PGD2 were
29 ocarcinoma A549 cells stably over-expressing TP receptor alpha isoform (A549-TPalpha).
30 s lost following stimulation of thromboxane (TP) receptors, an effect that may contribute to the endo
31              We propose that vasoconstrictor TP receptor and MaxiK-channel direct interaction facilit
32 eceptor knockout (TP-KO) mice or a selective TP receptor antagonist (SQ29,548), would alleviate LPS-i
33                   Treatment of mice with the TP receptor antagonist GR32191, alone or in combination
34 traction in arteries from males, whereas the TP receptor antagonist GR32191B inhibited the PVAT-induc
35 ist AL-8810, were uniformly abolished by the TP receptor antagonist SQ-29,548.
36 ur aim was to determine whether ifetroban, a TP receptor antagonist, attenuates aspirin-induced respi
37 y the residues involved in ligand binding, a TP receptor antagonist, SQ29,548 was used to interact wi
38 m treatment with S18886, an orally available TP receptor antagonist.
39 9548, a thromboxane/prostaglandin (PG) H(2) (TP) receptor antagonist, significantly reduced the incre
40 deposits, this was blocked by a thromboxane (TP) receptor antagonist, suggesting that TP receptor act
41 thromboxane A(2)/prostaglandin endoperoxide (TP) receptor antagonist, while 3',5'-diiodo-TMQ (2) exhi
42                                        Thus, TP receptor antagonists and TXA2 synthase inhibitors hav
43                                       DP and TP receptor antagonists at doses 5- to 20-fold greater t
44 uggest applications of antiplatelet drugs or TP receptor antagonists for the treatment of AERD.
45        The findings suggest applications for TP receptor antagonists in cases of asthma with high lev
46 r antagonists), BWA868c, and SQ29548 (DP and TP receptor antagonists, respectively) on the intraocula
47 nd TCC-SUP) with TXAS inhibitors and TXA(2) (TP) receptor antagonists reduced cell growth, migration,
48 h NO synthase inhibition, but is restored if TP receptors are blocked.
49 otoxemic shock induced by LPS is mediated by TP receptors as indicated by pharmacologic blockade and
50       Voltage sensitivity was not limited to TP receptor because prostaglandin F receptor activated w
51 ntrast, cardiac afferents, in the absence of TP receptor blockade responded consistently to repeated
52                  Contrary to our hypothesis, TP receptor blockade worsened aspirin-induced reactions
53                       Our data indicate that TP-receptor blockade with terutroban decreases portal pr
54  investigated whether terutroban, a specific TP receptor blocker, decreases hepatic vascular tone and
55 phosphorylation of both wild type and mutant TP receptors, but the extent of phosphorylation of the r
56 -terminal serines, and 3) desensitization of TP receptors by PKC is complex and involves mechanisms t
57 lightly lower affinity to both beta 2-AR and TP receptor compared to their diiodo analogs.
58 chaemia through direct activation of TxA(2) (TP) receptors coupled with the phospholipase C-protein k
59 ical functions of TP receptors, we generated TP receptor-deficient mice by gene targeting.
60                                              TP receptor-deficient mice had an approximately 2-fold i
61 CAM-1 and VCAM-1 in an aspirin-sensitive and TP receptor-dependent manner.
62 percentages of eosinophils in the blood by a TP receptor-dependent mechanism.
63 rol of platelet/granulocyte interactions and TP-receptor-dependent cysLT production, permitting MC ac
64  (DP(1)) or the thromboxane-like prostanoid (TP) receptor did not play a role in mediating the effect
65 e contraction by the TXA2 agonist U46619, or TP receptor expression in arteries from different sexes.
66 LISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expression determined by Western blotting.
67   To test the effectiveness of targeting the TP receptor for AD therapy, Tg2576 mice underwent long-t
68                                  Deletion of TP receptors from ptges(-/-) mice reduces inflammation,
69 ized thromboxane/prostaglandin endoperoxide (TP) receptors, from human platelets and rat vascular smo
70 ding to the eLP(2) (residues 173-193) of the TP receptor has been made with the N- and C-termini conn
71                                              TP receptors have been implicated in the pathogenesis of
72 inity to identify structural determinants of TP receptor heterogeneity.
73 ng little tonic influence of TxA(2) on renal TP receptors in health.
74                                  Conversely, TP receptors in the glomerulus may counteract the effect
75 d a key role for the thromboxane-prostanoid (TP) receptor in AERD.
76 2 (TxA2), we created a mutant TxA2 receptor (TP receptor) in which serines at positions 321, 322, and
77  receptor, 2) PKC-induced desensitization of TP receptors is caused, in part, by phosphorylation of C
78 to wild-type levels, with contributions from TP receptors localized to both hematopoietic cells and t
79                   Specific inhibition of the TP receptor may provide a more precise approach to limit
80 -46619 and 10-100 microM PGF(2alpha) cause a TP receptor-mediated Ca2+ influx involving both L-type C
81 ter oral administration, was able to prevent TP receptor-mediated platelet aggregation and to reduce
82                        Analysis of the human TP receptor model generated from molecular modeling base
83 embrane helices connecting the eLP(2) in the TP receptor model.
84 ugh activation of thromboxane A2-prostanoid (TP) receptors on neurons.
85 tage dependence of the thromboxane receptor (TP receptor) on the receptor level as well as on downstr
86 dial ischaemia through direct stimulation of TP receptors probably located in the cardiac sensory ner
87 Azide, was first shown to specifically label TP receptor protein.
88 ns of site direct mutagenesis, we identified TP receptor R295(7.40), which showed alteration of volta
89                               The absence of TP receptors reduced immune-mediated tissue injury follo
90                          We demonstrate that TP receptor regulation of APP expression depends on Galp
91        Thus, PGE(2) controls the strength of TP receptor signaling as a major bronchoprotective mecha
92 e Abeta, and APP levels, thereby implicating TP receptor signaling as a novel target for AD therapy.
93                                              TP receptor signaling ex vivo is controlled heterologous
94                                              TP receptor stimulation lead to loss of K(Ca)2.3 mediate
95  endothelial apoptosis, and inflammation via TP receptor stimulation.
96 GH(2) or other eicosanoids likely results in TP receptor stimulation.
97 ould be of significant value in the study of TP receptor structure and signaling.
98 dinated derivative 5, maintaining potency in TP receptor systems (112%) was coupled with maintaining
99  TMQ derivatives with significant potency in TP receptor systems (91%) and reduced potency in beta-ad
100 ork identified an amino acid sequence of the TP receptor that is directly involved in ligand binding.
101 In lung, thromboxane A2 (TXA2) activates the TP receptor to induce proinflammatory and bronchoconstri
102 nockout (KO)] or the thromboxane prostanoid (TP) receptor (TP KO).
103 ed by the equilibrium and kinetics of TP and TP receptor (TPR) binding, using electrokinetic concentr
104  showed alteration of voltage sensitivity of TP receptor upon mutation.
105  effective potential (V(0.5)) determined for TP receptor was -46 mV, which is within the physiologic
106 This agonist-specific phosphorylation of the TP receptor was largely prevented by inhibitors of PKC.
107 o investigate the physiological functions of TP receptors, we generated TP receptor-deficient mice by
108      Both hematopoietic and nonhematopoietic TP receptors were essential for LTC4 to induce eosinophi
109 chemical staining approach, we observed that TP receptors were expressed in cardiac sensory neurons i

 
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