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1 is mediated through the PGF2alpha receptor (FP receptor).
2 2alpha in cats is mediated by EP1 but not by FP receptor.
3 yocytes through the activation of endogenous FP receptors.
4 osomal PGE synthase-1 and EP1, EP2, EP3, and FP receptors.
5 melanocyte dendricity through EP1, EP3, and FP receptors.
6 odies to the EP(1), EP(2), EP(3), EP(4), and FP receptors.
7 ctural requirements for substrate binding to FP receptors.
8 ted sizes corresponding to the EP2, EP4, and FP receptors.
9 lls that was consistent with the presence of FP receptors.
10 WT mice via activation of the F prostanoid (FP) receptor.
12 gonist 17-phenyl trinor PGE2 and the partial FP receptor agonist AL-8810, were uniformly abolished by
14 o 0.1 microM PGF(2alpha) was mimicked by the FP receptor agonist fluprostenol, whilst the effect of 1
16 ly with prostaglandin F2alpha, fluprostenol (FP receptor agonist), or 17-phenyl trinor PGE2 (EP1 rece
17 as approximately equipotent to the selective FP receptor agonists fluprostenol and 17-phenyl PGF(2alp
18 iverse PGF(2alpha) structural analogs to the FP receptor and compared these with binding by the PG tr
19 PGF(2alpha) may compete for binding between FP receptors and PGT, these findings have implications f
20 1 expression after PGF(2alpha) activation of FP receptors and suggests that this could be an early ev
22 ained iberiotoxin (IbTX)-sensitive, AL-8810 (FP receptor antagonist)-insensitive BK channel currents
24 (PKC) inhibitor, chelerythrine chloride; the FP receptor antagonist, AL-8810; and the MEK inhibitor,
25 nhibition of FP receptor signalling with the FP receptor antagonist, chemical disruptors of the phosp
28 staglandin F2alpha (PGF2alpha) F prostanoid (FP) receptors are both potent regulators of blood pressu
30 in the omega chain increased binding to the FP receptor but reduced affinity for PGT, and substituti
32 We hypothesized that activation of the human FP receptor by PGF(2alpha) could induce the expression o
35 Swiss white mice (n = 17), which have normal FP receptor expression, provided the control population.
40 e characterized the expression of the EP and FP receptors in human melanocytes and show that human me
41 lities for GPCRs and suggest novel roles for FP receptors in normal tissue development and malignant
44 ken together, these results suggest that the FP receptor isoforms are coupled to at least two second
47 us studies have shown that the activation of FP receptors leads to phosphatidylinositol hydrolysis, i
52 showed conclusively the presence of EP4 and FP receptor messenger RNAs and proteins, respectively, i
55 he presence of high levels of both EP(1) and FP receptor mRNA transcripts in the blood vessels of iri
58 rabecular meshwork is mediated by prostanoid FP receptors (receptors for prostaglandin F2 alpha) in t
62 etrapeptide arg-gly-asp-ser or inhibition of FP receptor signalling with the FP receptor antagonist,
63 Fluprostenol, a specific activator of the FP receptor, significantly increased mineralization of O
64 oup was essential for optimal binding to the FP receptor, since replacement by larger moieties with a
66 uite different signal transduction pathways, FP receptor stimulation up-regulates CTGF and Cyr61.
69 at low concentrations of PGF(2alpha) act via FP receptors to cause IP3-dependent Ca2+ release and sto
70 The hybridization signals corresponding to FP receptor transcript were similar to those of EP(1) re
71 work cells were examined for the presence of FP receptors using immunofluorescence microscopy with af
73 nd neither did M1, except for activating the FP receptor with EC(50) = 557.9 +/- 55.2 nM (n = 4).
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