ライフサイエンスコーパス: prostaglandin E

1 we show that the G protein-coupled receptor prostaglandin E(1) (EP(1)) reduces the expression of COX

2 em delay affected the response to 3,7-dithia prostaglandin E(1) (PGE(1)).

3 nhibited by preincubating platelets with the prostaglandin E(1) or the ADP scavenger apyrase but was

4 ue were much higher than those obtained when prostaglandin E(1) was added to inhibit release or when

5 th mutated VP1u, increased the production of prostaglandin E(2) >100-fold.

6 of the endogenous PPAR-gamma ligand 15-keto-prostaglandin E(2) (15-keto-PGE(2)).

7 bone metastases produced significantly more prostaglandin E(2) (an important mediator of COX-2) than

8 lamin A accumulation, whereas treatment with prostaglandin E(2) (PGE(2) ) caused a marked increase in

9 Here, we investigate the function of prostaglandin E(2) (PGE(2) ) signaling through its EP3 r

10 The lipid mediator prostaglandin E(2) (PGE(2)) acts primarily as a proinfla

11 nduced signaling pathways, infection-induced prostaglandin E(2) (PGE(2)) also augmented COX-2 transcr

12 h cis-UCA resulted in increased synthesis of prostaglandin E(2) (PGE(2)) and cell death.

13 lishment of a positive feedback loop between prostaglandin E(2) (PGE(2)) and cyclooxygenase 2 (COX2),

14 Levels of prostaglandin E(2) (PGE(2)) and its processing enzyme, p

15 Eicosanoid lipid mediators, including prostaglandin E(2) (PGE(2)) and leukotrienes (LTs) B(4)

16 identified cyclooxygenase-2 (COX-2)-derived prostaglandin E(2) (PGE(2)) and lipoxin A(4) (LXA(4)) as

17 d (GCF) levels of interleukin (IL)-1beta and prostaglandin E(2) (PGE(2)) and serum levels of IL-6 wer

18 ovel cross-talk between the COX-2-controlled prostaglandin E(2) (PGE(2)) and Stat3 signaling pathways

19 LT production can be suppressed by prostaglandin E(2) (PGE(2)) and the cyclic AMP-dependent

20 Prostaglandin E(2) (PGE(2)) and VEGF levels in Muller ce

21 Elevated levels of prostaglandin E(2) (PGE(2)) are often found in colorecta

22 r activator of NF-kappaB ligand (RANK-L) and prostaglandin E(2) (PGE(2)) are two such molecules which

23 ve been associated with increased release of prostaglandin E(2) (PGE(2)) as a result of overexpressio

24 Interestingly, SphK1-knockout mice inhibited prostaglandin E(2) (PGE(2)) but not PGI(2) production in

25 Arachidonic acid is converted to prostaglandin E(2) (PGE(2)) by a sequential enzymatic re

26 e 2 (COX-2) overexpression and production of prostaglandin E(2) (PGE(2)) by head and neck squamous ce

27 ncisella tularensis induces the synthesis of prostaglandin E(2) (PGE(2)) by infected macrophages to a

28 tion of cyclooxygenases (COX) and release of prostaglandin E(2) (PGE(2)) by lung cells, including alv

29 majority of G protein-coupled receptors, the prostaglandin E(2) (PGE(2)) E-prostanoid 3 (EP3) recepto

30 Through the receptor EP4, prostaglandin E(2) (PGE(2)) exerts an anti-inflammatory

31 Although the lipid mediator prostaglandin E(2) (PGE(2)) exerts antifibrotic effects

32 ibroblast activation, and the lipid mediator prostaglandin E(2) (PGE(2)) exerts its well known anti-f

33 COX-2 inhibitor celecoxib reduces COX-2 and prostaglandin E(2) (PGE(2)) expression and adenomas in t

34 rted that toxin A increased cyclooxygenase-2/prostaglandin E(2) (PGE(2)) expression and apoptosis in

35 onstrate that C. albicans produces authentic prostaglandin E(2) (PGE(2)) from arachidonic acid.

36 cytoplasmic protein capable of metabolism of prostaglandin E(2) (PGE(2)) from the cyclooxygenase meta

37 The prostaglandin E(2) (PGE(2)) G protein-coupled receptor (

38 ing activated by fluid flow shear stress and prostaglandin E(2) (PGE(2)) had a stimulatory effect on

39 Cycloxygenase-2 (COX-2)-derived prostaglandin E(2) (PGE(2)) has been shown to be importa

40 The bioactive lipid mediator prostaglandin E(2) (PGE(2)) has been shown to exert a my

41 L)-6, tumor necrosis factor (TNF)-alpha, and prostaglandin E(2) (PGE(2)) in a dose-dependent manner b

42 detection assay, and levels of adenosine or prostaglandin E(2) (PGE(2)) in cell supernatants were an

43 e of this study was to determine the role of prostaglandin E(2) (PGE(2)) in modulating neuronal activ

44 (NO), tumor necrosis factor (TNF)-alpha, and prostaglandin E(2) (PGE(2)) in the AqH were determined.

45 ection also led to a significant increase of prostaglandin E(2) (PGE(2)) in the bronchoalveolar lavag

46 us reports, a peripheral injection of 0.1 mg prostaglandin E(2) (PGE(2)) into the intraplantar area o

47 Prostaglandin E(2) (PGE(2)) is a lipid mediator that act

48 Cyclooxygenase (COX)-derived prostaglandin E(2) (PGE(2)) is a prevalent and establish

49 Prostaglandin E(2) (PGE(2)) is an abundant lipid inflamm

50 Prostaglandin E(2) (PGE(2)) is an arachidonic acid metab

51 Prostaglandin E(2) (PGE(2)) is an inflammatory mediator

52 In the bone marrow, prostaglandin E(2) (PGE(2)) is known to affect both oste

53 Prostaglandin E(2) (PGE(2)) is one of the most ubiquitou

54 Cyclooxygenase-2-derived prostaglandin E(2) (PGE(2)) is produced at high levels i

55 Here, we show that prostaglandin E(2) (PGE(2)) is required for optimal Flt3

56 Because prostaglandin E(2) (PGE(2)) is the major UV-induced pros

57 al and genetic experiments, we now show that prostaglandin E(2) (PGE(2)) is the trophic signal requir

58 Prostaglandin E(2) (PGE(2)) is thought to play a role in

59 Cyclooxygenase-2 and prostaglandin E(2) (PGE(2)) levels are increased in colo

60 Mammary aromatase activity and prostaglandin E(2) (PGE(2)) levels were increased in mic

61 Prostaglandin E(2) (PGE(2)) mediates the masculinization

62 ynia, a subsequent intraplantar injection of prostaglandin E(2) (PGE(2)) or intrathecal injection of

63 nd sphingomyelin metabolites in the TNFalpha/prostaglandin E(2) (PGE(2)) pathway was investigated.

64 Prostaglandin E(2) (PGE(2)) plays a major role both in m

65 inhibited interleukin (IL)-1beta-stimulated prostaglandin E(2) (PGE(2)) production almost completely

66 a G-protein/Ca(2+) one that is required for prostaglandin E(2) (PGE(2)) production and bronchiolar s

67 Here we show that prostaglandin E(2) (PGE(2)) production by microsomal PGE

68 p27-specific small interfering RNA increased prostaglandin E(2) (PGE(2)) production in both unstimula

69 ncreased COX-2 protein, mRNA expression, and prostaglandin E(2) (PGE(2)) production was observed afte

70 It is noteworthy that prostaglandin E(2) (PGE(2)) production was significantly

71 hanges in Ca(2+) signaling, cell volume, and prostaglandin E(2) (PGE(2)) production were measured in

72 )gamma activity was monitored by quantifying prostaglandin E(2) (PGE(2)) production.

73 Prostaglandin E(2) (PGE(2)) promotes cancer progression

74 The effect of epinephrine on PAF-mediated prostaglandin E(2) (PGE(2)) release from human aortic sm

75 hibited larger currents as well as augmented prostaglandin E(2) (PGE(2)) release in response to two T

76 ond, treatment of NSCLC cells with exogenous prostaglandin E(2) (PGE(2)) significantly decreased the

77 Here we show that prostaglandin E(2) (PGE(2)) silences certain tumor-suppr

78 Cyclooxygenase-2-derived prostaglandin E(2) (PGE(2)) stimulates tumor cell growth

79 Inducible vascular prostaglandin E(2) (PGE(2)) synthesis by endothelial (EC

80 Decreased Prostaglandin E(2) (PGE(2)) synthesis due to interferenc

81 We recently reported the role of visfatin in prostaglandin E(2) (PGE(2)) synthesis in chondrocytes.

82 nflammatory mediators, such as cytokines and prostaglandin E(2) (PGE(2)) that are elevated in OA join

83 study was to identify the receptors (EP) for prostaglandin E(2) (PGE(2)) that mediate the induction o

84 production of the proinflammatory molecule, prostaglandin E(2) (PGE(2)) to produce sex-specific brai

85 proteinase-2 (MMP-2), nitric oxide (NO), and prostaglandin E(2) (PGE(2)) were determined in AqH by sp

86 ar fluid (GCF) interleukin-1beta (IL-1beta), prostaglandin E(2) (PGE(2)), 8-isoprostane (8-iso), and

87 High levels of prostaglandin E(2) (PGE(2)), a COX-2 product, were relea

88 Our data show that prostaglandin E(2) (PGE(2)), a factor overproduced in ch

89 r the biosynthesis of eicosanoids, including prostaglandin E(2) (PGE(2)), a key lipid mediator involv

90 human CD36 released severalfold more AA and prostaglandin E(2) (PGE(2)), a major product of AA metab

91 nt challenge by the proinflammatory cytokine prostaglandin E(2) (PGE(2)), a phenomenon known as hyper

92 immunosuppressive and antiapoptotic mediator prostaglandin E(2) (PGE(2)), a product of cyclooxygenase

93 Prostaglandin E(2) (PGE(2)), a proinflammatory bioactive

94 ase A(2) (PLA(2))-dependent rapid release of prostaglandin E(2) (PGE(2)), activation of protein kinas

95 nhibiting the LPS-induced nitric oxide (NO), prostaglandin E(2) (PGE(2)), and proinflammatory cytokin

96 cellular secretion of nitric oxide (NO) and prostaglandin E(2) (PGE(2)), as well as the mRNA level o

97 ia arising from inflammatory agents, such as prostaglandin E(2) (PGE(2)), can be antagonized by activ

98 ed induction of cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)), important mediators of infl

99 orted that the immunosuppressive eicosanoid, prostaglandin E(2) (PGE(2)), is capable of activating HP

100 Prostaglandin E(2) (PGE(2)), one of the downstream produ

101 Prostaglandin E(2) (PGE(2)), produced by M. tuberculosis

102 Prostaglandin E(2) (PGE(2)), the most abundant COX-2-der

103 Treatment with cis-UCA increased prostaglandin E(2) (PGE(2)), tumor necrosis factor-alpha

104 y the tumor-associated inflammatory mediator prostaglandin E(2) (PGE(2)), which attracts myeloid-deri

105 urated fatty acid (PUFA) arachidonic acid to prostaglandin E(2) (PGE(2)), which drives tumorigenesis;

106 ion of mfat-1 led to decreased production of prostaglandin E(2) (PGE(2)), which in turn contributed t

107 e gut and increased plasma concentrations of prostaglandin E(2) (PGE(2)), which induced M2 macrophage

108 These immune cells produce prostaglandin E(2) (PGE(2)), which influences adipocyte

109 , tumor necrosis factor alpha, and IL-6] and prostaglandin E(2) (PGE(2)), which is added to preserve

110 ose generation is induced by TLR ligation is prostaglandin E(2) (PGE(2)), which is well known to incr

111 ypoxia is accompanied by increased levels of prostaglandin E(2) (PGE(2)), which promote tumor cell su

112 Plasma membrane repair depended on prostaglandin E(2) (PGE(2)), which regulates synaptotagm

113 t, malignant breast epithelial cells secrete prostaglandin E(2) (PGE(2)), which stimulates aromatase

114 Prostaglandin E(2) (PGE(2))- and carbachol-stimulated mu

115 at norepinephrine synaptically mediates this Prostaglandin E(2) (PGE(2))-dependent change in temperat

116 For example, prostaglandin E(2) (PGE(2))-induced transactivation of t

117 yl]-N,N-d iethylbenzamide (SNC80) to inhibit prostaglandin E(2) (PGE(2))-stimulated adenylyl cyclase

118 COX-2 inhibitors that prevent production of prostaglandin E(2) (PGE(2)).

119 a, interleukin-10 (IL-10), nitric oxide, and prostaglandin E(2) (PGE(2)).

120 c effects of inflammatory mediators, such as prostaglandin E(2) (PGE(2)).

121 ygenase-2 (COX-2) and produce high levels of prostaglandin E(2) (PGE(2)).

122 rocess is mediated by its enzymatic product, prostaglandin E(2) (PGE(2)).

123 he presence of proinflammatory cytokines and prostaglandin E(2) (PGE(2)).

124 oxygenase (COX-2) and subsequent increase of prostaglandin E(2) (PGE(2)).

125 Cancer-stimulating factors (VEGF & prostaglandin E(2) [PGE(2)]) and levels of cAMP were mea

126 h iloprost, a prostaglandin I(2) analog, and prostaglandin E(2) abrogated the potent contractile resp

127 /EBP-beta, up-regulation of COX-2, increased prostaglandin E(2) accumulation, and activation of Wnt t

128 xpression and resultant inability to secrete prostaglandin E(2) after R. rickettsii infection.

129 prostaglandins, some of which (e.g. glyceryl prostaglandin E(2) and glyceryl prostaglandin I(2)) exhi

130 ibuted to the down-regulation of circulating prostaglandin E(2) and indoleamine 2, 3,-dioxygenase enz

131 e in the synthesis of the antifibrotic agent prostaglandin E(2) and is reduced in sarcoidosis lung.

132 d in decreased pro-inflammatory derivatives (prostaglandin E(2) and leukotriene B(4)) and an increase

133 ABA suppresses LPS-induced prostaglandin E(2) and MCP-1 production via a PPAR gamma

134 ttings of salt loading, urinary excretion of prostaglandin E(2) and nitrate/nitrite were remarkably i

135 Levels of prostaglandin E(2) and the prostaglandin-endoperoxide sy

136 nsitive to PAN-induced injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater

137 Prostaglandin E(2) and total nitrite levels were also de

138 C1, AC2, AC8, and AC9, and the receptors for prostaglandin E(2) and vasoactive intestinal polypeptide

139 Cyclic AMP, induced by agonists such as prostaglandin E(2) and vasoactive intestinal polypeptide

140 idation, and stimulated an early increase in prostaglandin E(2) at the infarct site.

141 GES-1), encoded by the Ptges gene, catalyzes prostaglandin E(2) biosynthesis and is expressed by leuk

142 cytes negatively regulates COX-1 expression, prostaglandin E(2) biosynthesis, and inflammation in the

143 Prostaglandin E(2) blocks transforming growth factor TGF

144 Valdecoxib reduced basal brain prostaglandin E(2) concentrations at dosages that did no

145 increase in Cox-2 mRNA abundance and reduced prostaglandin E(2) content compared with adenomas from t

146 Recent studies demonstrate that the prostaglandin E(2) EP2 receptor is a major regulator of

147 RvD1 reduced prostaglandin E(2) generation from CRECs.

148 , to produce tolerance for its inhibition of prostaglandin E(2) hyperalgesia, simultaneously produced

149 colons and is concomitant with a doubling of prostaglandin E(2) in 15-PGDH null colonic mucosa.

150 the paraventricular nucleus of hypothalamus, prostaglandin E(2) in cerebrospinal fluid, and Fra-like

151 nase/AKT, beta-catenin, and cyclooxygenase-2/prostaglandin E(2) in HCA7 colon carcinoma cells.

152 forms differentially inhibit COX-2-catalyzed prostaglandin E(2) in IL-1beta-stimulated A549 cells wit

153 significantly reduced the concentrations of prostaglandin E(2) in ischemic penumbral cortex as compa

154 tractant protein-1, and cyclooxygenase-2 and prostaglandin E(2) in LPS-activated RAW264.7 murine macr

155 Gastric epithelial cells liberate prostaglandin E(2) in response to cytokines as part of t

156 Herein, we show by genetic intervention that prostaglandin E(2) in the spinal cord is mainly produced

157 Prostaglandin E(2) levels in cerebrospinal fluid were no

158 Intrapancreatic prostaglandin E(2) levels were reduced in nimesulide-fed

159 ety, survival, change in cerebrospinal fluid prostaglandin E(2) levels, and changes in the rate of de

160 sociated gastritis despite decreased gastric prostaglandin E(2) levels.

161 evelop PHO secondary to chronically elevated prostaglandin E(2) levels.

162 Delta 18 COX-2 mice do have elevated urinary prostaglandin E(2) metabolite levels and display a more

163 The urinary prostaglandin E(2) metabolite, which is a biomarker of p

164 n hyperalgesia evoked by local injections of prostaglandin E(2) or epinephrine.

165 Proinflammatory prostaglandin E(2) plays an important role in cancer ini

166 The EP(3) receptor on the platelet mediates prostaglandin E(2) potentiation of thrombogenic coagonis

167 Prostaglandin E(2) produced by the tumor cell plays a cr

168 PUFAs was negatively correlated with urinary prostaglandin E(2) production (r = -0.18; P = 0.002).

169 uction of COX2 was associated with increased prostaglandin E(2) production and podocyte death, both o

170 inflammatory compounds identified to inhibit prostaglandin E(2) production differed from those involv

171 e for calcium-induced fatty acid release and prostaglandin E(2) production from cPLA(2) alpha(-/-) lu

172 ovalbumin, salmon parvalbumin, or Derp1 and prostaglandin E(2) production in response to lipopolysac

173 a is an important mediator of AA release and prostaglandin E(2) production in SMCs, modulating vascul

174 production, cyclooxygenase-2 expression, and prostaglandin E(2) production were also significantly de

175 Cyclooxygenase (Cox)-2 and prostaglandin E(2) production were analyzed by real-time

176 esponsible for induction of Cox-2, increased prostaglandin E(2) production, and activation of EGFR si

177 din E(2) metabolite, which is a biomarker of prostaglandin E(2) production, was measured in 896 parti

178 the induction of cyclooxygenase (COX)-2, and prostaglandin E(2) production.

179 tion of cyclooxygenase (COX)-2 and increased prostaglandin E(2) production.

180 Here we report that prostaglandin E(2) promotes renal cancer cell invasion t

181 arget is selective suppression of microglial prostaglandin E(2) receptor subtype 2 (EP2) function, wh

182 omboxane B(2), and had greater expression of prostaglandin E(2) receptor subtype 4 (EP(4)) and thromb

183 m2/m3 muscarinic acetylcholine receptors or prostaglandin E(2) receptors were not affected by either

184 hypertonic NaCl, in parallel with increased prostaglandin E(2) release.

185 significantly reduced, whereas production of prostaglandin E(2) remained unchanged.

186 Further, we show that prostaglandin E(2) secretion in the lung is responsible

187 These observations expand the roles of prostaglandin E(2) signaling in metabolic regulation bey

188 These data suggest that prostaglandin E(2) signaling via the EP2 receptor functi

189 number of studies have identified cytosolic prostaglandin E(2) synthase (cPGES)/p23 as a cytoplasmic

190 Microsomal prostaglandin E(2) synthase-1 (mPGES-1), encoded by the

191 in the IL-1beta-induced COX-2 expression and prostaglandin E(2) synthesis and might represent a novel

192 Suppression occurred primarily through prostaglandin E(2) synthesis in MAPCs, which resulted in

193 ll proliferation and GVHD-induced injury via prostaglandin E(2) synthesis in vivo.

194 molecular levels reveal that KLF11 inhibits prostaglandin E(2) synthesis via transcriptional silenci

195 Increased levels of COX-2 mRNA, protein, and prostaglandin E(2) synthesis were detected in HPV16 E6-

196 enzymatic activity as well as COX-2 mRNA and prostaglandin E(2) synthesis, activating both NFkappaB a

197 ndent increase in cyclooxygenase 1-dependent prostaglandin E(2) synthesis.

198 8 expression was dependent on COX-2-mediated prostaglandin E(2) synthesis.

199 e in ovarian cyclooxygenase 1 expression and prostaglandin E(2) synthesis.

200 NF-alpha) reprogram macrophages by releasing prostaglandin E(2) that acts on the macrophages through

201 he marked reduction in the amount of adipose prostaglandin E(2) that binds the Galpha(i)-coupled rece

202 the activation of TLRs and the production of prostaglandin E(2) through COX-2, has protective effects

203 Levels of prostaglandin E(2) were higher in the infarct and viable

204 les (IL-10, transforming growth factor-beta, prostaglandin E(2)) in the tumor microenvironment.

205 r signal-regulated kinase)-regulated PGE(2) (prostaglandin E(2)) signaling mechanism, maintain neuron

206 -2) and induced the synthesis and release of prostaglandin E(2), a potent vasodilator and classic par

207 direct treatment of brain microvessels with prostaglandin E(2), a product of COX-2 activity, resulte

208 ich was partially overcome when treated with prostaglandin E(2), a product of cyclooxygenase (COX)-2

209 tion in AQP1(-/-) mice evoked by bradykinin, prostaglandin E(2), and capsaicin as well as reduced col

210 ssion, and the production of IL-6, IL-8, and prostaglandin E(2), and the matrix metalloproteinases MM

211 d cells of nociceptor sensitizers, including prostaglandin E(2), bradykinin, and nerve growth factor,

212 intra-articular Ca(2+) ionophore ionomycin, prostaglandin E(2), cAMP-raising agents, serine/threonin

213 nhibitory G-proteins (G(s) to G(i)), and for prostaglandin E(2), emergence of novel dependence on pro

214 Prostaglandin E(2), Escherichia coli heat-stable enterot

215 suggesting a role for prostanoids, including prostaglandin E(2), in differentiation of regulatory CD1

216 ependent of transforming growth factor beta, prostaglandin E(2), interleukin (IL)-10, and thymic stro

217 Apoptotic PMN gave elevated prostaglandin E(2), lipoxin B(4) and RvE2, whereas zymos

218 P activity, and inhibited IL-1beta-activated prostaglandin E(2), matrix metalloproteinase 3, IL-6, IL

219 a variety of inflammatory mediators such as prostaglandin E(2), nitric oxide, IL-1beta and matrix me

220 of MG63 cells grown on SLA and modSLA [e.g., prostaglandin E(2), osteoprotegerin, latent and active T

221 f markers of inflammation (cyclooxygenase-2, prostaglandin E(2), proliferating cell nuclear antigen,

222 s exhibited significant increases in retinal prostaglandin E(2), superoxide, vascular endothelial gro

223 de dismutase-1 mutation led to the idea that prostaglandin E(2), the main synthetic product of Cox-2,

224 Recent findings suggest that the prostaglandin E(2), the proinflammatory product of eleva

225 IL)-1beta, IL-6, matrix metalloproteinase-8, prostaglandin E(2), tumor necrosis factor-alpha, interfe

226 how that transforming growth factor-beta and prostaglandin E(2), two immunosuppressive tumor-derived

227 the downregulation of Akt, cyclooxygenase-2, prostaglandin E(2), vascular endothelial growth factor,

228 Prostaglandin E(2), which exerts its functions by bindin

229 fining hyaluronan-dependent cyclooxygenase-2/prostaglandin E(2)-associated signaling pathways will pr

230 In conclusion, the prostaglandin E(2)-EP4 signaling pathway plays a role in

231 ockdown of PKA-alpha decreased forskolin- or prostaglandin E(2)-stimulated phosphorylation of FoxO1.

232 rotic cell death by inhibiting production of prostaglandin E(2).

233 tivation of MAPKs, COX-2, and the release of prostaglandin E(2).

234 y either COX-2-derived prostaglandin I(2) or prostaglandin E(2).

235 s)-dependent receptors for isoproterenol and prostaglandin E(2).

236 el occurs through a mechanism independent of prostaglandin E(2).

237 ic release of arachidonate and production of prostaglandin E(2).

238 sitization of TRPV1 induced by forskolin and prostaglandin E(2).

239 s the ethanol extract mitigated secretion of prostaglandin E(2).

240 art through a reduction in the production of prostaglandin E(2).

241 were stimulated with interleukin-1 beta and prostaglandin E(2).

242 These findings have revealed a mPGES-1/prostaglandin E(2)/NO/cGMP pathway that appears to be cr

243 station was analyzed for C-reactive protein; prostaglandin E(2); matrix metalloproteinase-9; fibrinog

244 aging G93A SOD mice, genetic deletion of the prostaglandin E(2)EP2 receptor improved motor strength a

245 s, LPS strongly induced COX-2 and microsomal prostaglandin-E(2) (PGE(2)) synthase-1, mediated by the

246 Levels of prostaglandins E(2) (PGE(2)), F(2alpha) (PGF(2alpha)), l

247 R3 in phagocytes was caused by inhibition of prostaglandin E-2 (PGE-2) levels, which were significant

248 evel of n-3 fatty acids and their metabolite prostaglandin E(3) (PGE(3)) were much higher (but the n-

249 ha(z) signaling pathway, through circulating prostaglandin E activating the EP3 isoform of the E pros

250 These results show that the prostaglandin E/beta-arrestin 1/c-Src signaling complex

251 atory enzymes that mediate the production of prostaglandins (e.g. cyclooxygenase-2) and leukotrienes

252 Binding was not observed to other prostaglandins (e.g. PGE(1), PGE(2), 8-iso-PGF(2alpha),

253 Prostaglandin E (PGE) induced a robust inhibition of bot

254 Microsomal prostaglandin E (PGE) synthase-1 (mPGES-1) is an inducib

255 Bisulfite sequencing of the prostaglandin E receptor 2 gene (PTGER2) promoter reveal

256 expression profiling and identified PTGER2 (prostaglandin E receptor 2) as a target gene of HB9 in a

257 relation between a specific polymorphism of prostaglandin E receptor 3 (a gene associated with infla

258 s, we observed that Pgter3, the gene for the prostaglandin E receptor 3 (EP3), was upregulated with d

259 ort that PGE(2) induces the association of a prostaglandin E receptor 4/beta-arrestin 1/c-Src signali

260 Prostaglandin E Receptor EP1 transfection or treatment w

261 e used this model to examine the role of the prostaglandin E receptor subtype 4 (EP4) and genetic kno

262 Results show that only prostaglandin E receptor-4 (EP4) was involved and mediat

263 Prostaglandin E receptor-4 receptor mediates endothelial

264 demonstrates how heterodimerization between prostaglandin E receptors and beta(2)-adrenergic recepto

265 uodenal bicarbonate secretion is mediated by prostaglandin E receptors and stimulated by the prostone

266 The prostaglandin E synthase (PGES) responsible for acid-ind

267 bacterial growth, we show that infection of prostaglandin E synthase (PGES)(-/-) macrophages in vitr

268 terference with the Cyclooxygenase (Cox) and Prostaglandin E synthase (Ptges) enzymes halts gastrulat

269 g carcinoma cells reveal that Gas6 increases prostaglandin E synthase (Ptges) expression in endotheli

270 By contrast, deletion of microsomal prostaglandin E synthase 1 (mPGES-1) confers analgesia,

271 Global deletion of microsomal prostaglandin E synthase 1 (mPGES-1) in mice attenuates

272 Microsomal prostaglandin E synthase 1 (mPGES-1) is a key enzyme of

273 Microsomal prostaglandin E synthase 1 (mPGES-1) is an alpha-helical

274 type I receptor (IL-1RI), COX-2, microsomal prostaglandin E synthase 1 (mPGES-1), and EP receptors,

275 ymes cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase 1 (mPGES-1).

276 )), cyclooxygenase 2 (COX-2), and microsomal prostaglandin E synthase 1 (mPGES1).

277 otein phosphatase 2A (I1PP2A and I2PP2A) and prostaglandin E synthase 3 (PGES3)) were selected for va

278 expression was coupled to the expression of prostaglandin E synthase family members.

279 An x-ray study indicated that microsomal prostaglandin E synthase type 2 (mPGES2) is a heme-bound

280 PTGES, which encodes the prostaglandin E synthase, has also been linked to asthma

281 oma tumors express high levels of microsomal prostaglandin E synthase-1 (mPGES-1) and elevated levels

282 g of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) by a yet unknown me

283 Microsomal prostaglandin E synthase-1 (mPGES-1) in myeloid and vasc

284 tion of a virus vector expressing microsomal prostaglandin E synthase-1 (mPGES-1) into the median pre

285 Microsomal prostaglandin E synthase-1 (mPGES-1) is a key enzyme tha

286 Microsomal prostaglandin E synthase-1 (mPGES-1) is a rate-limiting

287 es in rats have demonstrated that microsomal prostaglandin E synthase-1 (mPGES-1) is induced in brain

288 creening hit was found to inhibit microsomal prostaglandin E synthase-1 (mPGES-1) with an IC50 of 17.

289 Microsomal prostaglandin E synthase-1 (mPGES-1), a membrane-associa

290 d with altered PGE(2) metabolism, microsomal prostaglandin E synthase-1 (mPGES-1), prostaglandin dehy

291 on of cyclooxygenase 2 (COX2) and microsomal prostaglandin E synthase-1 (mPGES-1), which are involved

292 xpression of cyclooxygenase-2 and microsomal prostaglandin E synthase-1 and reduces 15-hydroxyprostag

293 Inhibiting COX-2 or microsomal prostaglandin E synthase-1 suppressed the 6-OHDA-trigger

294 m of COX-1 that synthesizes PgE2 (microsomal prostaglandin E synthase-1) depends critically for its v

295 Cyclooxygenase (COX)-2 and microsomal prostaglandin E synthase-1, key components of the most w

296 nase, and of cyclooxygenase-2 and microsomal prostaglandin E synthase-1, key enzymes in the PGE(2) sy

297 landin E synthases, including membrane-bound prostaglandin E synthase-1.

298 clooxygenases (COX-1 and COX-2) and terminal prostaglandin E synthases (cPGES, mPGES-1, and mPGES-2).

299 Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Braf(V600E) mouse melanoma

300 e secretion is mediated by multiple types of prostaglandin E synthases, including membrane-bound pros