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1 lecular pharmacogenetic studies of the human prostacyclin receptor.
2 even-transmembrane (TM) domains of the human prostacyclin receptor.
3 s were not similarly altered in mice lacking prostacyclin receptors.
4 /2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.
5 he release of prostacyclin and activation of prostacyclin receptors.
6 the antagonists of EP4, prostaglandin D2, or prostacyclin receptors.
7 eceptors, respectively, with and without the prostacyclin receptor agonist iloprost.
8 ase stimulators, prostacyclin analogues, and prostacyclin receptor agonists.
9  it failed to activate the recombinant human prostacyclin receptor and caused only minimal activation
10 ha, Csf1) were increased by treatment with a prostacyclin receptor antagonist and protein kinase A in
11           Treatment of wild-type mice with a prostacyclin receptor antagonist or a peroxisome prolife
12 PGI2 binding to platelets was due to an anti-prostacyclin receptor antibody present in SCI plasma.
13 aining the structural integrity of the human prostacyclin receptor, as 7 of 12 extracellular and tran
14                     RMICs do not express the prostacyclin receptor, but they do express the prostacyc
15 most comprehensive characterization of human prostacyclin receptor genetic variants to date.
16 induced phosphorylation of an epitope-tagged prostacyclin receptor (HAhIP) is mediated primarily by P
17                      An epitope-tagged human prostacyclin receptor (HAhIP) was constructed and stably
18                                    The human prostacyclin receptor (hIP) has recently been recognized
19                                    The human prostacyclin receptor (hIP) is a seven transmembrane-spa
20 n = 1,761) to search for dysfunctional human prostacyclin receptor (hIP) variants, we recently discov
21                                    The human prostacyclin receptor (hIP), a G protein-coupled recepto
22 usters (analysis via a rhodopsin-based human prostacyclin receptor homology model).
23 .3 microM; n2 = 1772 +/- 226 sites per cell) prostacyclin receptor in normal platelets.
24  those seen in response to activation of the prostacyclin receptor IP.
25 athways involving a cyclooxygenase-2 (COX-2)/prostacyclin receptor (IP receptor) autocrine loop and a
26 first intracellular loop (iLP1) of the human prostacyclin receptor (IP) and G alpha s protein have be
27                             In contrast, the prostacyclin receptor (IP) mediates the inhibitory effec
28 ellular loop (iLP1, residues 39-51) of human prostacyclin receptor (IP) was proposed to be involved i
29 P), the thromboxane A2 receptor (TP) and the prostacyclin receptor (IP).
30                                    The human prostacyclin receptor is a seven-transmembrane alpha-hel
31 n the cyclooxygenase-2 inhibition studies or prostacyclin receptor knockout mice studies.
32        These results indicate that the human prostacyclin receptor may be regulated by agonist-depend
33                   Polymorphisms of the human prostacyclin receptor potentially may be important predi
34 e binding of [3H]prostaglandin E1, used as a prostacyclin receptor probe, showed the presence of one
35 ical approaches, we conclude that diminished prostacyclin receptor signaling may contribute, in part,
36 smembrane-located cysteine residues in human prostacyclin receptor structure-function.
37                     In the case of the human prostacyclin receptor, such alterations may reduce the c
38         Using multiple strategies, including prostacyclin receptor-targeted small interfering RNA, we
39                             We report that a prostacyclin receptor variant (R212C) is defective in ad
40 ion instigated further genetic screening for prostacyclin receptor variants on 1455 human genomic sam
41 in endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAM
42  Using a naturally occurring mutation in the prostacyclin receptor, we report for the first time that

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