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1 lecular pharmacogenetic studies of the human prostacyclin receptor.
2 even-transmembrane (TM) domains of the human prostacyclin receptor.
3  limit platelet reactivity by activating the prostacyclin receptor.
4 /2, cyclooxygenase COX-1 (but not COX-2) and prostacyclin receptors.
5 he release of prostacyclin and activation of prostacyclin receptors.
6 s were not similarly altered in mice lacking prostacyclin receptors.
7 the antagonists of EP4, prostaglandin D2, or prostacyclin receptors.
8                                     However, prostacyclin receptor activated with iloprost showed no
9 eceptors, respectively, with and without the prostacyclin receptor agonist iloprost.
10 ase stimulators, prostacyclin analogues, and prostacyclin receptor agonists.
11  it failed to activate the recombinant human prostacyclin receptor and caused only minimal activation
12 ha, Csf1) were increased by treatment with a prostacyclin receptor antagonist and protein kinase A in
13           Treatment of wild-type mice with a prostacyclin receptor antagonist or a peroxisome prolife
14 PGI2 binding to platelets was due to an anti-prostacyclin receptor antibody present in SCI plasma.
15 s are activated upon depolarization, whereas prostacyclin receptors are not.
16 aining the structural integrity of the human prostacyclin receptor, as 7 of 12 extracellular and tran
17 ccelerated thrombosis to a similar extent as prostacyclin receptor blockade.
18                     RMICs do not express the prostacyclin receptor, but they do express the prostacyc
19 most comprehensive characterization of human prostacyclin receptor genetic variants to date.
20 induced phosphorylation of an epitope-tagged prostacyclin receptor (HAhIP) is mediated primarily by P
21                      An epitope-tagged human prostacyclin receptor (HAhIP) was constructed and stably
22                                    The human prostacyclin receptor (hIP) has recently been recognized
23                                    The human prostacyclin receptor (hIP) is a seven transmembrane-spa
24 n = 1,761) to search for dysfunctional human prostacyclin receptor (hIP) variants, we recently discov
25                                    The human prostacyclin receptor (hIP), a G protein-coupled recepto
26 usters (analysis via a rhodopsin-based human prostacyclin receptor homology model).
27 .3 microM; n2 = 1772 +/- 226 sites per cell) prostacyclin receptor in normal platelets.
28  those seen in response to activation of the prostacyclin receptor IP.
29 athways involving a cyclooxygenase-2 (COX-2)/prostacyclin receptor (IP receptor) autocrine loop and a
30 first intracellular loop (iLP1) of the human prostacyclin receptor (IP) and G alpha s protein have be
31                             In contrast, the prostacyclin receptor (IP) mediates the inhibitory effec
32 ellular loop (iLP1, residues 39-51) of human prostacyclin receptor (IP) was proposed to be involved i
33 5b-KOs showed ex vivo significantly enhanced prostacyclin receptor (IP)-dependent relaxation, whereas
34 P), the thromboxane A2 receptor (TP) and the prostacyclin receptor (IP).
35                                    The human prostacyclin receptor is a seven-transmembrane alpha-hel
36 n the cyclooxygenase-2 inhibition studies or prostacyclin receptor knockout mice studies.
37        These results indicate that the human prostacyclin receptor may be regulated by agonist-depend
38       CS585 was shown to potently target the prostacyclin receptor on the human platelet, resulting i
39                   Polymorphisms of the human prostacyclin receptor potentially may be important predi
40 e binding of [3H]prostaglandin E1, used as a prostacyclin receptor probe, showed the presence of one
41 study, we identified the prostaglandin I(2) (prostacyclin) receptor PTGIR as a cell-intrinsic regulat
42 ical approaches, we conclude that diminished prostacyclin receptor signaling may contribute, in part,
43 smembrane-located cysteine residues in human prostacyclin receptor structure-function.
44                     In the case of the human prostacyclin receptor, such alterations may reduce the c
45         Using multiple strategies, including prostacyclin receptor-targeted small interfering RNA, we
46 R7 ligation coordinated with Galphas-coupled prostacyclin receptor to trigger cyclic adenosine monoph
47                             We report that a prostacyclin receptor variant (R212C) is defective in ad
48 ion instigated further genetic screening for prostacyclin receptor variants on 1455 human genomic sam
49 in endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAM
50  Using a naturally occurring mutation in the prostacyclin receptor, we report for the first time that