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1 ct was abrogated by an antagonist of the DP1 prostanoid receptor.
2  indomethacin or by null mutation of the EP3 prostanoid receptor.
3 mmatory properties attributed to the various prostanoid receptors.
4 n the signaling potential of EP(2) and EP(4) prostanoid receptors.
5 ect effect of PGs on specific ciliary muscle prostanoid receptors.
6 ical effects by binding to and activating FP prostanoid receptors.
7 clase activity, presumably via activation of prostanoid receptors.
8 in) rather than the decreased sensitivity of prostanoid receptors.
9 9 possess high selectivity relative to other prostanoid receptors.
10 al and uterine smooth-muscle cells via EP(3) prostanoid receptors.
11 hat these effects are not mediated via known prostanoid receptors.
12 with chemoattractant receptors compared with prostanoid receptors.
13                                            D prostanoid receptor 1 (DP(1)) or the thromboxane-like pr
14                                       Hence, prostanoid receptor-1 and tumour necrosis factor-alpha a
15                          Cyclooxygenase-2 or prostanoid receptor-1 inhibition reduced tumour necrosis
16                            Cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha in
17 tion or suppression of downstream molecules--prostanoid receptor-1 or tumour necrosis factor-alpha--m
18 treated with inhibitors of cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha; a
19 ssion of cyclooxygenase-2, prostaglandin E2, prostanoid receptor-1, tumour necrosis factor-alpha and
20                                        The D prostanoid receptor 2 (DP2; also known as chemoattractan
21 cy and interaction of the newly introduced E-prostanoid receptor 2 (EP2) agonists, rho-kinase inhibit
22 his is mediated by a cyclooxygenase-PGE(2)-E prostanoid receptor 2 (EP2)-adenylyl cyclase-cyclic AMP
23 h2 cells by signaling through its receptor E-prostanoid receptor 2 (EP2).
24                                            E-prostanoid receptor 2 agonists outperformed other non-PG
25                However, cyclooxygenase-1 and prostanoid receptor 2-4 levels were comparable in pups w
26 eated DC was mediated predominantly by the E prostanoid receptor 2.
27 GE2, which induces IL-1beta production via E prostanoid receptor 2/4-cAMP-PKA-NFkappaB-dependent mech
28             Inhibition of the PG receptors E-prostanoid receptors 2 and 4 prevented the tolerogenic e
29 t prostaglandin E2 signalling via the E-type prostanoid receptor 4 (EP4) on IECs represses epithelial
30 pholipase A2alpha that drives ciliary E-type prostanoid receptor 4 (EP4) signaling to ensure PC funct
31 oid prostaglandin E2 (PGE2) receptor, E-type prostanoid receptor 4 (EP4), mimicked effects seen with
32                                We find the E prostanoid receptor 4 expressed in T-ALL samples and dem
33        Recently we have shown that the FP(B) prostanoid receptor, a G-protein-coupled receptor that c
34 a), specific activators/inhibitors of the EP prostanoid receptors, a specific activator of the FP pro
35  cAMP-dependent protein kinase subsequent to prostanoid receptor activation.
36                                              Prostanoid receptor agonists and the combination thereof
37 ptors for prostaglandin E2 (PGE2) and that E-prostanoid receptor agonists, including PGE2, induce the
38 ooxygenase-2 inhibition or deletion of its I prostanoid receptor also predisposes to accelerated athe
39 xpression of the G(alphas) protein-coupled I prostanoid receptor and greater cAMP generation in PMs t
40                                        The D-prostanoid receptor and the chemoattractant receptor hom
41 , we studied mice with selective deletion of prostanoid receptors and generated conditionally immorta
42  insights into the structure and function of prostanoid receptors and may facilitate the development
43 on is the first that may be applied to other prostanoid receptors and other GPCRs.
44 xygenase-2, its derivative prostaglandin E2, prostanoid receptors and pro-inflammatory cytokines were
45 roblasts (18Co) through Gs protein-coupled E-prostanoid receptors and the cyclic AMP/protein kinase A
46 id receptors, a specific activator of the FP prostanoid receptor, and direct activators/inhibitors of
47 ere reversed by cyclooxygenase inhibition or prostanoid receptor antagonism.
48 y PGD2, while the selective thromboxane-like prostanoid receptor antagonist SQ29548 was without effec
49    Ramatroban, a dual CRTH2/thromboxane-like prostanoid receptor antagonist, markedly inhibited Th2 c
50 yclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinfla
51                                    Selective prostanoid receptor antagonists may provide new therapeu
52 landin E activating the EP3 isoform of the E prostanoid receptor, appears to be up-regulated in insul
53 ted moderate selectivity to EP2 over the DP1 prostanoid receptor ( approximately 10-fold) and low aqu
54 inked and peroxisomal proliferator-activated prostanoid receptors are expressed in both of these cell
55                                           FP prostanoid receptors are G-protein-coupled receptors (GP
56                                           FP prostanoid receptors are G-protein-coupled receptors tha
57                                           FP prostanoid receptors are G-protein-coupled receptors who
58 ibitory approach to perform the screening of prostanoid receptors as potential candidates that mediat
59 anner, 3) exhibits high selectivity over all prostanoid receptors as well as 157 other receptors and
60 hese clusters are highly conserved among the prostanoid receptors as well as other class A GPCRs.
61   Thromboxane A(2) receptor (TP receptor), a prostanoid receptor, belongs to the G protein-coupled re
62  of prostanoid synthesis or highly selective prostanoid receptor blockade.
63 I), containing the highly conserved (100% of prostanoid receptors) D288(7.49)/P289(7.50) motif locate
64 roduction of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis
65  with a family of distinct G protein-coupled prostanoid receptors designated EP, FP, IP, TP, and DP,
66         While BF cultures expressed all four prostanoid receptors, direct addition of sulprostone but
67 therapy could be targeted through a specific prostanoid receptor downstream of COX-2.
68  it functions through two major receptors, D prostanoid receptor (DP) and chemoattractant receptor-li
69 inflammatory responses by interaction with D prostanoid receptor (DP) and chemoattractant receptor-li
70 but its action and the roles of the 2 D-type prostanoid receptors (DPs) DP1 and DP2 (also called chem
71 ffect of pharmacological inactivation of the prostanoid receptor EP(4), one of the PGE(2) receptors,
72 n both cav and noncav fractions, whereas the prostanoid receptors EP(2)R and EP(4)R were excluded fro
73 ittle is known about other aspects of E-type prostanoid receptor (EP) 1 receptor signaling.
74 re mediated by the combined action of E-type prostanoid receptor (EP) 2 and EP4 receptors, which were
75 einyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signa
76 lls were transfected with the Ca2+-coupled E-prostanoid receptor EP1 (HEK/EP1) and loaded with fura-2
77 a class of four distinct G-protein-coupled E-prostanoid receptors (EP1-EP4) that have divergent effec
78      It is known that PGE2 signals via the E prostanoid receptors, EP1-4, but the role that each rece
79                                              Prostanoid receptor EP2 can play a proinflammatory role,
80                                          The prostanoid receptor EP2 was overexpressed in human prost
81 ed to the expression of IL-6 mediated by the prostanoid receptor EP2.
82                                Agonists of E prostanoid receptors EP2 (butaprost) and EP1/3 (sulprost
83 e show the ERG-mediated up-regulation of the prostanoid receptors EP2 and EP3.
84  isolated from obese-diabetic mice expressed prostanoid receptors, EP2 and DP1, and contained signifi
85   Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R(-/-) mice) exhibit increa
86 nflammatory lipid mediator that binds four E prostanoid receptors (EPs 1 to 4).
87 fferent functions and cell distribution of E prostanoid receptors explain the difficulty encountered
88                       Finally, analysis of E prostanoid receptor expression and their selective inhib
89 l assays with respect to most members of the prostanoid receptor family and a more modest 30- to 50-f
90              CRTH2 is the only member of the prostanoid receptor family that is phylogenetically dist
91 PRC5B physically interacts with GPCRs of the prostanoid receptor family, resulting in enhanced signal
92 In vivo studies validating multitargeting of prostanoid receptors for achieving superior anti-inflamm
93 ty of Ishikawa cells stably expressing the F-prostanoid receptor (FPS) to adhere to vitronectin.
94 promising new outlook for the examination of prostanoid receptor-G-protein interactions in greater de
95 e pairs (kb) in length and, like other known prostanoid receptor genes, contains three exons and two
96 tion than that of the first introns of other prostanoid receptor genes.
97               By contrast, deletion of the I prostanoid receptor had no effect on the attenuation of
98         The intrarenal distribution of these prostanoid receptors has been mapped, and the consequenc
99                                           FP prostanoid receptors have been identified as two isoform
100 se data strongly imply that the endogenous E prostanoid receptor in the Ins-1(832/13) beta-cell line
101 ropathic rats, and may suggest a role for IP prostanoid receptors in pain episodes associated with ne
102                             Other intrarenal prostanoid receptors include the PGF2 alpha receptor (FP
103 n, a strategy to identify and block specific prostanoid-receptor interactions may be required.
104 ilator properties of PGI2, deletion of the I prostanoid receptor (Ipr) suppressed this response.
105                                      The EP1 prostanoid receptor is one of four subtypes whose cognat
106                  Here we show that the EP(3) prostanoid receptor is specifically activated by ricinol
107                                        An FP prostanoid receptor isoform, which appears to arise from
108 gulation of second messenger signaling by FP prostanoid receptor isoforms.
109 h regenerative potential, of which EP and IP prostanoid receptor ligands had the most profound therap
110  suggests that the iLP1 regions of the other prostanoid receptors may also contain the epitopes impor
111  obesity and suggest that targeting specific prostanoid receptors may represent a novel strategy for
112 er augmented by coincident deletion of the I prostanoid receptor (n=10-18).
113 n affinity consistent with an interaction at prostanoid receptors of the EP(2)-subtype.
114 ons demonstrate the first working example of prostanoid receptor polypharmacology for potentially saf
115                           Through the use of prostanoid receptor sequence alignments, site-directed m
116              COXs, prostanoid synthases, and prostanoid receptors should provide fruitful targets for
117 n, and we now suggest how targeting specific prostanoid receptor signaling pathways could be exploite
118 nhibited by beta-cyclodextrin treatment, but prostanoid receptor-stimulated AC activity, which appear
119 t-induced desensitization of secretin and IP-prostanoid receptor-stimulated adenylyl cyclase was not
120 t-induced desensitization of secretin and IP-prostanoid receptor-stimulated adenylyl cyclase was the
121 broblasts; (ii) PGE(2) activation of the EP3 prostanoid receptor stimulates the activation of JNK.
122 dating the role of prostaglandin E2 (PGE2) E-prostanoid receptor subtype 1 (EP1) in regulating blood
123                               In contrast, E-prostanoid receptor subtype 2 (EP2) activation, which se
124             Here, we show that ablation of E prostanoid receptor subtype 2 (EP2) significantly increa
125           These data indicate that the EP(4) prostanoid receptor subtype, but not the EP(2), couples
126 ion of mRNA encoding two PGE(2) receptors, E-prostanoid receptor subtypes 2 and 4, as well as each re
127                          The EP(2) and EP(4) prostanoid receptor subtypes are G-protein-coupled recep
128                           Cooperativity of E-prostanoid receptor subtypes in regulating signaling and
129  levels was detected for the EP(3) and EP(4) prostanoid receptor subtypes in tissue sections or prima
130 sic residues (Arg45 in the IP) in all of the prostanoid receptors suggests that the iLP1 regions of t
131 receptor pathways, beta(2)-adrenoceptors and prostanoid receptors that are expressed endogenously in
132 product of arachidonic acid that activates D prostanoid receptors to modulate vascular, platelet, and
133 ion of PGI2, we generated mice lacking the I prostanoid receptor together with mPges-1 on a hyperlipi
134 ion of the vasoconstricting thromboxane A(2) prostanoid receptor (TP), a mechanism supported by MaxiK
135 hromboxane A2 synthase (TxA2-S), thromboxane prostanoid receptors (TP-Rs), or superoxide anion (O2-)
136 bset of GABAergic neurons that express the E-prostanoid receptor type 3.
137     Whereas compounds selective for a single prostanoid receptor typically exhibited modest but stati
138 ighly conserved extracellular domains of the prostanoid receptors were found in the second extracellu
139       We now report that the EP(2) and EP(4) prostanoid receptors, which couple to Galpha(s), also ac
140  effect was due to the loss of high-affinity prostanoid receptors, which may contribute to atherogene
141 as due to the loss of platelet high-affinity prostanoid receptors, which may contribute to atherogene
142 se findings reveal that blockade of multiple prostanoid receptors, with absent antagonism of EP2 and
143                   Multitargeting of selected prostanoid receptors yielded a prototype compound, compo

 
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