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

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

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

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

7 A special regulatory role for prostaglandin E(2) (PGE(2) ) has been postulated in nons

8 Furthermore, measurement of prostaglandin E(2) (PGE(2) ) levels in plasma from patie

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

10 -catenin signaling, cyclooxygenase-2 (COX-2)/prostaglandin E(2) (PGE(2) ) signaling, and the apeliner

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 adult human lung fibroblasts, but found that prostaglandin E(2) (PGE(2)) and fibroblast growth factor

15 Both prostaglandin E(2) (PGE(2)) and hypoxia-inducible factor

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

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

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

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

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

28 Reduced levels of prostaglandin E(2) (PGE(2)) contribute to aspirin-induce

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 of fentanyl and confirmed by prolongation of prostaglandin E(2) (PGE(2)) hyperalgesia.

42 europlasticity manifested as prolongation of prostaglandin E(2) (PGE(2)) hyperalgesia.

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

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

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

46 ndin dehydrogenase (HPGD), which catabolizes prostaglandin E(2) (PGE(2)) into the metabolite 15-keto

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 Elevated prostaglandin E(2) (PGE(2)) levels are observed in color

60 5a) during MCC fate choice, where modulating prostaglandin E(2) (PGE(2)) levels rescued MCC number.

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 trate that MDV infection activates the COX-2/prostaglandin E(2) (PGE(2)) pathway, as evident by incre

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

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

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

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

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

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

70 Prostaglandin E(2) (PGE(2)) promotes colorectal tumor fo

71 g monocytes and macrophages, which can cause prostaglandin E(2) (PGE(2)) release and consequently und

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

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

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

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

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

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

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

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

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

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

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

83 ulation-specific changes in sensitization by prostaglandin E(2) (PGE(2)) were observed, when compared

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

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

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

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

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

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

90 Receptors for leukotriene B(4) (LTB(4)), prostaglandin E(2) (PGE(2)), and SPMs are expressed on l

91 xpression of inflammatory mediators, such as prostaglandin E(2) (PGE(2)), bradykinin (BK), and nerve

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

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

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

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

96 sphoprotein (p-VASP) by isoproterenol (ISO), prostaglandin E(2) (PGE(2)), or forskolin (FSK) as well

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

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

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

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

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

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

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

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

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

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

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

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

109 tumorigenicity of GSCs through production of prostaglandin E(2) (PGE(2)), which stimulates beta-caten

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

111 xyprostaglandin dehydrogenase (15-PGDH), the prostaglandin E(2) (PGE(2))-degrading enzyme, as a hallm

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

113 oid 2-arachidonoylglycerol (2-AG) to produce prostaglandin E(2) (PGE(2))-glycerol (PGE(2)-G); PGE(2)-

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

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

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

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

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

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

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

121 process arachidonic acid into highly labile prostaglandin E(2) (PGE(2)).

122 so called COX2) to increase the synthesis of prostaglandin E(2) (PGE2) by mast cells, which activates

123 , we hypothesized that inhibiting microsomal prostaglandin E(2) (PGE2) synthase-1 (mPGES-1), the enzy

124 iators, like tumor necrosis factor-alpha and prostaglandin E(2) , increased by LPS-induced EP, were d

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 ts confirmed that silencing of MGL decreases prostaglandin E(2) accumulation in the intestine and up-

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

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

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

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

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

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

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

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

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

140 Pharmacological blockade of prostaglandin E(2) biosythesis favors CD103(+) dendritic

141 e outcome of drug-induced ICD and pose COX-2/prostaglandin E(2) blockade as a strategy to harness ICD

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

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

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

145 R4 AS-ODN) prevented OIH and prolongation of prostaglandin E(2) hyperalgesia (priming) induced by LDM

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

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

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

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

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

151 mice, and this was associated with decreased prostaglandin E(2) in plasma and skin.

152 cell carcinoma, ASA reduced plasma and skin prostaglandin E(2) levels and indices of UVB-induced DNA

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

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

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

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

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

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

159 nts in MCs triggered to migration by IL-8 or prostaglandin E(2) or to FcepsilonRI-stimulated secretio

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

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

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

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

164 ion, which is caused by reduced hypothalamic prostaglandin E(2) production and increased heat loss in

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

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

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

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

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

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

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

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

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

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

175 t and concentration-dependent suppression of prostaglandin E(2) production.

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

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

178 glandin F receptor activated with U46619 and prostaglandin E(2) receptor subtype 3 activated with ilo

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

180 activation of prostaglandin F receptors and prostaglandin E(2) receptors as well as thromboxane rece

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

182 ies reveal gemcitabine concurrently triggers prostaglandin E(2) release as an inhibitory DAMP to coun

183 IL-1beta treatment induced profound prostaglandin E(2) release in AR compared with AT cells.

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

185 plication of MGO together with bradykinin or prostaglandin E(2) resulted in an overadditive effect on

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

187 ase 4D (PDE4D) activity to amplify autocrine prostaglandin E(2) signaling in airway smooth muscle cel

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

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

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

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

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

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

197 8 expression was dependent on COX-2-mediated prostaglandin E(2) synthesis.

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

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

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

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

202 and an aberrant dependency on COX-1-derived prostaglandin E(2) to maintain a tenuous homeostasis.

203 eries of small-molecule full agonists of the prostaglandin E(2) type 4 (EP(4)) receptor have been gen

204 ule sensing, a competitive FP immunoassay of Prostaglandin E(2) was demonstrated using the developed

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

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

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

208 CRs agonists, including thrombin, histamine, prostaglandin E(2), and ADP, stimulated robust p38 autop

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

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

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

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

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

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

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

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

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

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

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

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

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

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 tation and host fitness through TGF-beta and prostaglandin E(2).

235 ake of arachidonic acid and the synthesis of prostaglandin E(2).

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

237 daptation might be dependent on TGF-beta and prostaglandin E(2).

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

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

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

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

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

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

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

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

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

247 aspirin decreased nasal symptoms and urinary prostaglandin E metabolite (P < 0.05) and increased urin

248 oup was accompanied by a decrease in urinary prostaglandin E metabolite levels (-27% +/- 7%; p = 0.01

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

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

251 Although prostaglandin E receptor (EP)-2 and EP4 for PGE2 are cou

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

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

254 ersus a combination of inflammation (PTGER2 [prostaglandin E receptor 2] and IL-6) plus growth/repair

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

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

257 Prostaglandin E Receptor EP1 transfection or treatment w

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

259 trated that cyclooxygenase-2 (COX-2) and the prostaglandin E receptor, prostanoid E receptor subtype

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

261 Prostaglandin E receptor-4 receptor mediates endothelial

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

263 ether PPI treatment affects NOX5, microsomal prostaglandin E synthase (mPGES)-1 and inducible nitric

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

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

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

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

268 in-endoperoxide synthase 2 (Ptgs2/Cox-2) and prostaglandin E synthase (Ptges/mPGES-1) was compromised

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

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

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

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

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

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

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

276 Finally, reduced prostaglandin E synthase 2 (PGES2) levels were found in

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

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

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

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

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

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

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

296 RNAi knockdown of microsomal prostaglandin E synthase-1, the rate-limiting enzyme in

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