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1 hromboxane A2 elicits scratching through its TP receptor.
2 ossible ligand-binding sites on native human TP receptor.
3 extra- and the intracellular domains of the TP receptor.
4 macologic blockade and genetic disruption of TP receptors.
5 t responsiveness of wild type but not mutant TP receptors.
6 abolished binding affinity at beta 2-AR and TP receptors.
7 thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor.
8 A(2) and signaling through the T prostanoid (TP) receptor.
9 he gene encoding the thromboxane-prostanoid (TP) receptor.
10 tic and lung tissue-associated T prostanoid (TP) receptors.
11 elet-adherent granulocytes and T-prostanoid (TP) receptors.
12 by G protein-coupled thromboxane-prostanoid (TP) receptors.
13 s to agonist-specific desensitization of the TP receptor, 2) PKC-induced desensitization of TP recept
16 ted by cell culture studies that showed that TP receptor activation increased Abeta and secreted APP
17 ne (TP) receptor antagonist, suggesting that TP receptor activation mediates the effects of iPF(2alph
19 lter beta 2-AR affinity, but greatly reduced TP receptor affinity (380- and 1200-fold, respectively).
25 s lost following stimulation of thromboxane (TP) receptors, an effect that may contribute to the endo
27 eceptor knockout (TP-KO) mice or a selective TP receptor antagonist (SQ29,548), would alleviate LPS-i
29 traction in arteries from males, whereas the TP receptor antagonist GR32191B inhibited the PVAT-induc
31 y the residues involved in ligand binding, a TP receptor antagonist, SQ29,548 was used to interact wi
33 9548, a thromboxane/prostaglandin (PG) H(2) (TP) receptor antagonist, significantly reduced the incre
34 deposits, this was blocked by a thromboxane (TP) receptor antagonist, suggesting that TP receptor act
35 thromboxane A(2)/prostaglandin endoperoxide (TP) receptor antagonist, while 3',5'-diiodo-TMQ (2) exhi
39 r antagonists), BWA868c, and SQ29548 (DP and TP receptor antagonists, respectively) on the intraocula
40 nd TCC-SUP) with TXAS inhibitors and TXA(2) (TP) receptor antagonists reduced cell growth, migration,
42 otoxemic shock induced by LPS is mediated by TP receptors as indicated by pharmacologic blockade and
43 ntrast, cardiac afferents, in the absence of TP receptor blockade responded consistently to repeated
45 investigated whether terutroban, a specific TP receptor blocker, decreases hepatic vascular tone and
46 phosphorylation of both wild type and mutant TP receptors, but the extent of phosphorylation of the r
47 -terminal serines, and 3) desensitization of TP receptors by PKC is complex and involves mechanisms t
49 chaemia through direct activation of TxA(2) (TP) receptors coupled with the phospholipase C-protein k
53 rol of platelet/granulocyte interactions and TP-receptor-dependent cysLT production, permitting MC ac
54 (DP(1)) or the thromboxane-like prostanoid (TP) receptor did not play a role in mediating the effect
55 e contraction by the TXA2 agonist U46619, or TP receptor expression in arteries from different sexes.
56 LISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expression determined by Western blotting.
57 To test the effectiveness of targeting the TP receptor for AD therapy, Tg2576 mice underwent long-t
59 ized thromboxane/prostaglandin endoperoxide (TP) receptors, from human platelets and rat vascular smo
60 ding to the eLP(2) (residues 173-193) of the TP receptor has been made with the N- and C-termini conn
65 2 (TxA2), we created a mutant TxA2 receptor (TP receptor) in which serines at positions 321, 322, and
66 receptor, 2) PKC-induced desensitization of TP receptors is caused, in part, by phosphorylation of C
67 to wild-type levels, with contributions from TP receptors localized to both hematopoietic cells and t
69 -46619 and 10-100 microM PGF(2alpha) cause a TP receptor-mediated Ca2+ influx involving both L-type C
73 dial ischaemia through direct stimulation of TP receptors probably located in the cardiac sensory ner
78 e Abeta, and APP levels, thereby implicating TP receptor signaling as a novel target for AD therapy.
84 dinated derivative 5, maintaining potency in TP receptor systems (112%) was coupled with maintaining
85 TMQ derivatives with significant potency in TP receptor systems (91%) and reduced potency in beta-ad
86 ork identified an amino acid sequence of the TP receptor that is directly involved in ligand binding.
88 ed by the equilibrium and kinetics of TP and TP receptor (TPR) binding, using electrokinetic concentr
89 This agonist-specific phosphorylation of the TP receptor was largely prevented by inhibitors of PKC.
90 o investigate the physiological functions of TP receptors, we generated TP receptor-deficient mice by
92 chemical staining approach, we observed that TP receptors were expressed in cardiac sensory neurons i
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