ライフサイエンスコーパス: prostanoid receptor

1 indomethacin or by null mutation of the EP3 prostanoid receptor.

2 n the signaling potential of EP(2) and EP(4) prostanoid receptors.

3 ect effect of PGs on specific ciliary muscle prostanoid receptors.

4 ical effects by binding to and activating FP prostanoid receptors.

5 clase activity, presumably via activation of prostanoid receptors.

6 in) rather than the decreased sensitivity of prostanoid receptors.

7 al and uterine smooth-muscle cells via EP(3) prostanoid receptors.

8 hat these effects are not mediated via known prostanoid receptors.

9 mmatory properties attributed to the various prostanoid receptors.

10 with chemoattractant receptors compared with prostanoid receptors.

11 D prostanoid receptor 1 (DP(1)) or the thromboxane-like pr

12 Hence, prostanoid receptor-1 and tumour necrosis factor-alpha a

13 Cyclooxygenase-2 or prostanoid receptor-1 inhibition reduced tumour necrosis

14 Cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha in

15 tion or suppression of downstream molecules--prostanoid receptor-1 or tumour necrosis factor-alpha--m

16 treated with inhibitors of cyclooxygenase-2, prostanoid receptor-1 or tumour necrosis factor-alpha; a

17 ssion of cyclooxygenase-2, prostaglandin E2, prostanoid receptor-1, tumour necrosis factor-alpha and

18 The D prostanoid receptor 2 (DP2; also known as chemoattractan

19 his is mediated by a cyclooxygenase-PGE(2)-E prostanoid receptor 2 (EP2)-adenylyl cyclase-cyclic AMP

20 h2 cells by signaling through its receptor E-prostanoid receptor 2 (EP2).

21 However, cyclooxygenase-1 and prostanoid receptor 2-4 levels were comparable in pups w

22 eated DC was mediated predominantly by the E prostanoid receptor 2.

23 GE2, which induces IL-1beta production via E prostanoid receptor 2/4-cAMP-PKA-NFkappaB-dependent mech

24 Inhibition of the PG receptors E-prostanoid receptors 2 and 4 prevented the tolerogenic e

25 Recently we have shown that the FP(B) prostanoid receptor, a G-protein-coupled receptor that c

26 a), specific activators/inhibitors of the EP prostanoid receptors, a specific activator of the FP pro

27 cAMP-dependent protein kinase subsequent to prostanoid receptor activation.

28 Prostanoid receptor agonists and the combination thereof

29 ptors for prostaglandin E2 (PGE2) and that E-prostanoid receptor agonists, including PGE2, induce the

30 ooxygenase-2 inhibition or deletion of its I prostanoid receptor also predisposes to accelerated athe

31 xpression of the G(alphas) protein-coupled I prostanoid receptor and greater cAMP generation in PMs t

32 The D-prostanoid receptor and the chemoattractant receptor hom

33 , we studied mice with selective deletion of prostanoid receptors and generated conditionally immorta

34 on is the first that may be applied to other prostanoid receptors and other GPCRs.

35 xygenase-2, its derivative prostaglandin E2, prostanoid receptors and pro-inflammatory cytokines were

36 roblasts (18Co) through Gs protein-coupled E-prostanoid receptors and the cyclic AMP/protein kinase A

37 id receptors, a specific activator of the FP prostanoid receptor, and direct activators/inhibitors of

38 ere reversed by cyclooxygenase inhibition or prostanoid receptor antagonism.

39 y PGD2, while the selective thromboxane-like prostanoid receptor antagonist SQ29548 was without effec

40 Ramatroban, a dual CRTH2/thromboxane-like prostanoid receptor antagonist, markedly inhibited Th2 c

41 yclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinfla

42 Selective prostanoid receptor antagonists may provide new therapeu

43 landin E activating the EP3 isoform of the E prostanoid receptor, appears to be up-regulated in insul

44 ted moderate selectivity to EP2 over the DP1 prostanoid receptor ( approximately 10-fold) and low aqu

45 inked and peroxisomal proliferator-activated prostanoid receptors are expressed in both of these cell

46 FP prostanoid receptors are G-protein-coupled receptors (GP

47 FP prostanoid receptors are G-protein-coupled receptors tha

48 FP prostanoid receptors are G-protein-coupled receptors who

49 ibitory approach to perform the screening of prostanoid receptors as potential candidates that mediat

50 anner, 3) exhibits high selectivity over all prostanoid receptors as well as 157 other receptors and

51 hese clusters are highly conserved among the prostanoid receptors as well as other class A GPCRs.

52 Thromboxane A(2) receptor (TP receptor), a prostanoid receptor, belongs to the G protein-coupled re

53 of prostanoid synthesis or highly selective prostanoid receptor blockade.

54 I), containing the highly conserved (100% of prostanoid receptors) D288(7.49)/P289(7.50) motif locate

55 roduction of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis

56 with a family of distinct G protein-coupled prostanoid receptors designated EP, FP, IP, TP, and DP,

57 While BF cultures expressed all four prostanoid receptors, direct addition of sulprostone but

58 therapy could be targeted through a specific prostanoid receptor downstream of COX-2.

59 it functions through two major receptors, D prostanoid receptor (DP) and chemoattractant receptor-li

60 inflammatory responses by interaction with D prostanoid receptor (DP) and chemoattractant receptor-li

61 but its action and the roles of the 2 D-type prostanoid receptors (DPs) DP1 and DP2 (also called chem

62 ffect of pharmacological inactivation of the prostanoid receptor EP(4), one of the PGE(2) receptors,

63 n both cav and noncav fractions, whereas the prostanoid receptors EP(2)R and EP(4)R were excluded fro

64 ittle is known about other aspects of E-type prostanoid receptor (EP) 1 receptor signaling.

65 re mediated by the combined action of E-type prostanoid receptor (EP) 2 and EP4 receptors, which were

66 einyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signa

67 lls were transfected with the Ca2+-coupled E-prostanoid receptor EP1 (HEK/EP1) and loaded with fura-2

68 a class of four distinct G-protein-coupled E-prostanoid receptors (EP1-EP4) that have divergent effec

69 It is known that PGE2 signals via the E prostanoid receptors, EP1-4, but the role that each rece

70 Prostanoid receptor EP2 can play a proinflammatory role,

71 The prostanoid receptor EP2 was overexpressed in human prost

72 ed to the expression of IL-6 mediated by the prostanoid receptor EP2.

73 Agonists of E prostanoid receptors EP2 (butaprost) and EP1/3 (sulprost

74 e show the ERG-mediated up-regulation of the prostanoid receptors EP2 and EP3.

75 isolated from obese-diabetic mice expressed prostanoid receptors, EP2 and DP1, and contained signifi

76 Adult mice carrying a null mutation of the prostanoid receptor EP3R (EP3R(-/-) mice) exhibit increa

77 fferent functions and cell distribution of E prostanoid receptors explain the difficulty encountered

78 Finally, analysis of E prostanoid receptor expression and their selective inhib

79 l assays with respect to most members of the prostanoid receptor family and a more modest 30- to 50-f

80 In vivo studies validating multitargeting of prostanoid receptors for achieving superior anti-inflamm

81 ty of Ishikawa cells stably expressing the F-prostanoid receptor (FPS) to adhere to vitronectin.

82 promising new outlook for the examination of prostanoid receptor-G-protein interactions in greater de

83 e pairs (kb) in length and, like other known prostanoid receptor genes, contains three exons and two

84 tion than that of the first introns of other prostanoid receptor genes.

85 By contrast, deletion of the I prostanoid receptor had no effect on the attenuation of

86 The intrarenal distribution of these prostanoid receptors has been mapped, and the consequenc

87 FP prostanoid receptors have been identified as two isoform

88 se data strongly imply that the endogenous E prostanoid receptor in the Ins-1(832/13) beta-cell line

89 ropathic rats, and may suggest a role for IP prostanoid receptors in pain episodes associated with ne

90 Other intrarenal prostanoid receptors include the PGF2 alpha receptor (FP

91 n, a strategy to identify and block specific prostanoid-receptor interactions may be required.

92 The EP1 prostanoid receptor is one of four subtypes whose cognat

93 Here we show that the EP(3) prostanoid receptor is specifically activated by ricinol

94 An FP prostanoid receptor isoform, which appears to arise from

95 gulation of second messenger signaling by FP prostanoid receptor isoforms.

96 suggests that the iLP1 regions of the other prostanoid receptors may also contain the epitopes impor

97 obesity and suggest that targeting specific prostanoid receptors may represent a novel strategy for

98 er augmented by coincident deletion of the I prostanoid receptor (n=10-18).

99 n affinity consistent with an interaction at prostanoid receptors of the EP(2)-subtype.

100 ons demonstrate the first working example of prostanoid receptor polypharmacology for potentially saf

101 Through the use of prostanoid receptor sequence alignments, site-directed m

102 COXs, prostanoid synthases, and prostanoid receptors should provide fruitful targets for

103 n, and we now suggest how targeting specific prostanoid receptor signaling pathways could be exploite

104 nhibited by beta-cyclodextrin treatment, but prostanoid receptor-stimulated AC activity, which appear

105 t-induced desensitization of secretin and IP-prostanoid receptor-stimulated adenylyl cyclase was not

106 t-induced desensitization of secretin and IP-prostanoid receptor-stimulated adenylyl cyclase was the

107 broblasts; (ii) PGE(2) activation of the EP3 prostanoid receptor stimulates the activation of JNK.

108 dating the role of prostaglandin E2 (PGE2) E-prostanoid receptor subtype 1 (EP1) in regulating blood

109 In contrast, E-prostanoid receptor subtype 2 (EP2) activation, which se

110 Here, we show that ablation of E prostanoid receptor subtype 2 (EP2) significantly increa

111 These data indicate that the EP(4) prostanoid receptor subtype, but not the EP(2), couples

112 ion of mRNA encoding two PGE(2) receptors, E-prostanoid receptor subtypes 2 and 4, as well as each re

113 The EP(2) and EP(4) prostanoid receptor subtypes are G-protein-coupled recep

114 levels was detected for the EP(3) and EP(4) prostanoid receptor subtypes in tissue sections or prima

115 sic residues (Arg45 in the IP) in all of the prostanoid receptors suggests that the iLP1 regions of t

116 receptor pathways, beta(2)-adrenoceptors and prostanoid receptors that are expressed endogenously in

117 product of arachidonic acid that activates D prostanoid receptors to modulate vascular, platelet, and

118 ion of PGI2, we generated mice lacking the I prostanoid receptor together with mPges-1 on a hyperlipi

119 ion of the vasoconstricting thromboxane A(2) prostanoid receptor (TP), a mechanism supported by MaxiK

120 hromboxane A2 synthase (TxA2-S), thromboxane prostanoid receptors (TP-Rs), or superoxide anion (O2-)

121 bset of GABAergic neurons that express the E-prostanoid receptor type 3.

122 Whereas compounds selective for a single prostanoid receptor typically exhibited modest but stati

123 ighly conserved extracellular domains of the prostanoid receptors were found in the second extracellu

124 We now report that the EP(2) and EP(4) prostanoid receptors, which couple to Galpha(s), also ac

125 effect was due to the loss of high-affinity prostanoid receptors, which may contribute to atherogene

126 as due to the loss of platelet high-affinity prostanoid receptors, which may contribute to atherogene

127 se findings reveal that blockade of multiple prostanoid receptors, with absent antagonism of EP2 and

128 Multitargeting of selected prostanoid receptors yielded a prototype compound, compo