ライフサイエンスコーパス: PGF2alpha

1 PGF2alpha also activates the extracellular signal-regula

2 PGF2alpha also induced eIF4E and 4E-BP1 phosphorylation,

3 PGF2alpha and the PG mixture at 25 muM concentration sig

4 PGF2alpha induced the activities of extracellular signal

5 PGF2alpha-induced phosphorylation of eIF4E and 4E-BP1 wa

6 PGF2alpha-induced up-regulation of Cyr61 appeared to exc

7 ertrophic agonists in culture, endothelin-1, PGF2alpha, and phorbol 12-myristate 13-acetate, also ind

8 cosanoids analyzed, tetranor-PGEM and 11beta-PGF2alpha as well as 11-dehydro-TXB2 showed a significan

9 Prostaglandin (15R-PGF2alpha, 11B-dhk-PGF2alpha) and linoleic acid derivati

10 in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation appea

11 deposition (MMP9), and prostanoids (PGE(2), PGF2alpha, TXA2) were all more effectively reduced by na

12 1alpha (PGF1alpha), prostaglandin F(2alpha) (PGF2alpha), and prostaglandin D2 (PGD2).

13 However, the TP receptor agonists U-46,619, PGF2alpha, and PGD2 were more potent than PGE2.

14 d decreased myometrial NF-kappaB activation, PGF2alpha, and expression of contraction-associated gene

15 ted amniotic fluid IL-1beta, IL-6, IL-8, and PGF2alpha, resulting in PTB and marked neonatal mortalit

16 ane B2 (TXB2 ) were quantified by ELISA, and PGF2alpha (FP) and thromboxane A2 (TP) receptor expressi

17 novel functions for parasite-derived LBs and PGF2alpha in the cellular metabolism of Leishmania and i

18 The amount of parasite LBs and PGF2alpha were modulated by exogenous arachidonic acid.

19 rations of TXB2 (stable TXA2 metabolite) and PGF2alpha , soluble cell adhesion molecules and blood pr

20 ther cycloxygenase products, PGE2, PGD2, and PGF2alpha, failed to activate p38 kinase in aspirin-trea

21 Thus, the ratio of endogenous PGE2 and PGF2alpha has the potential to selectively regulate one

22 tion, PGHS-2, and the production of PGE2 and PGF2alpha.

23 sanoids, such as prostaglandin E2 (PGE2) and PGF2alpha, precedes the onset of labor as a result of in

24 taglandin profile: TxB2>6-keto PGF1alpha and PGF2alpha>PGE2, despite the comparable release of total

25 so-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.

26 tural specificity versus 8-epi PGF3alpha and PGF2alpha.

27 Recombinant trout Tnfalpha (rTnfalpha) and PGF2alpha recapitulate the stimulatory in vitro effects

28 the cyclooxygenase products thromboxane and PGF2alpha are released from coronary artery PVAT from pi

29 identified as 8-isoPGF2alpha, 5iPF2 VI, and PGF2alpha based on their retention times and MS/MS spect

30 of inositol phosphates to the same extent as PGF2alpha in cells expressing either the FPA or FPB isof

31 of FPB-expressing cells with PGE2-attenuated PGF2alpha-stimulated Tcf/beta-catenin signaling in a dos

32 The primary outcomes 2,3-dinor-11-beta-PGF2alpha, GETE score, and standard clinical biomarkers

33 Both PGF2alpha and 8,12-iso-iPF2alpha-III activate the p70S6

34 Both PGF2alpha and Bimatoprost up-regulated Cyr61 mRNA expres

35 Thus, both PGF2alpha and 8,12-iso-iPF2alpha-III induce myocyte hype

36 ed the intraocular pressure response to both PGF2alpha and 17-phenyl trinor PGE2.

37 We show that NFAT is activated by PGF2alpha, and the isoform NFATC2 is required for PGF2al

38 had little or no effect on the NPV caused by PGF2alpha or LY83583.

39 n of intraocular pressure in cats induced by PGF2alpha is mediated by FP or other prostaglandin recep

40 n synthesis and bFGF-2 expression induced by PGF2alpha.

41 he expression of which is also stimulated by PGF2alpha.

42 In cardiomyocytes, PGF2alpha increases the hydrolysis of inositol phosphate

43 ntraocular pressure, indicating that in cats PGF2alpha and 17-phenyl trinor PGE2 act on the same rece

44 d PORH and increased TXA2 but did not change PGF2alpha levels.

45 urition initiation via COX1 and COX2 derived PGF2alpha leveraging epithelial specific Shp2 knockout m

46 We detected PGF2alpha receptor (FP) on the Leishmania PV surface.

47 Prostaglandin (15R-PGF2alpha, 11B-dhk-PGF2alpha) and linoleic acid derivatives (12,13 EpOME) a

48 lowing luteolysis in the absence of elevated PGF2alpha production.

49 the four Gq/Gi-coupled receptors [EP1, EP3, PGF2alpha (FP), thromboxane A2 (TP)] suggests that prost

50 8-epi PGF2alpha and IPF2alpha-I are F2-isoprostanes produced i

51 Our results indicate that 8-epi PGF2alpha and IPF2alpha-I, two distinct F2-isoprostanes

52 istent with the enzymatic formation of 8-epi PGF2alpha by cyclooxygenases.

53 idly metabolized to inactive products, 8-epi PGF2alpha circulates in plasma.

54 e blockade by thromboxane antagonists, 8-epi PGF2alpha does not activate either of the thromboxane re

55 Furthermore, the response to 8-epi PGF2alpha exhibits structural specificity versus 8-epi P

56 8-epi PGF2alpha immunoreactivity was also detected in cells po

57 receptor by systemic concentrations of 8-epi PGF2alpha is unlikely to occur, even in syndromes of exc

58 8-Epi PGF2alpha may amplify the response to platelet agonists

59 8-epi PGF2alpha ranged from 1.310-3.450 pmol/micromol phosphol

60 the plaque were markedly positive for 8-epi PGF2alpha.

61 Much higher concentrations of 8-epi-PGF2alpha (10-20 microM) alone induce weak, reversible a

62 ute MI (105+/-17.8 versus 230+/-66 for 8-epi-PGF2alpha [P=.009] and 466+/-91 versus 833+/-153 for IPF

63 dural values by 24 hours (122+/-18 for 8-epi-PGF2alpha and 457+/-102 for IPF2alpha-I).

64 atosus had higher urinary excretion of 8-epi-PGF2alpha and IPF2alpha -I than controls; urinary excret

65 urinary excretion of two isoprostanes, 8-epi-PGF2alpha and IPF2alpha -I, free radical catalyzed oxida

66 (r=.68, P<.0001; n=33) between urinary 8-epi-PGF2alpha and IPF2alpha-I levels in patients receiving t

67 structurally distinct F2 isoprostanes, 8-epi-PGF2alpha and IPF2alpha-I.

68 Thus, 8-epi-PGF2alpha does not compete for binding at the stably exp

69 on, human monocytes may form bioactive 8-epi-PGF2alpha either via free radical- or enzyme-catalyzed p

70 Concentrations of 8-epi-PGF2alpha in the range 1 nM to 1 microM induce a dose-de

71 8-Epi-PGF2alpha is a more abundant product of monocyte PG G/H

72 There was a slight increase in urinary 8-epi-PGF2alpha levels (64.7+/-9.5 versus 84.9+/-10.6; P=.02)

73 Urinary 8-epi-PGF2alpha was highly correlated with both aCL titer (Rho

74 No difference of 8-epi-PGF2alpha was observed between patients with and without

75 compounds, 8-epiprostaglandin F2alpha (8-epi-PGF2alpha), is a mitogen and vasoconstrictor.

76 (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the utility of monitoring

77 ocytes resulted in marked formation of 8-epi-PGF2alpha, but not of PGE2 or TxB2.

78 ith L 745,337, suppressed formation of 8-epi-PGF2alpha, thiobarbituric acid-reactive substances, and

79 a (TNFalpha) and prostaglandin (PG) F2alpha (PGF2alpha) are involved in the control of ovulation but

80 n (NPV) stimulated by prostaglandin F2alpha (PGF2alpha ) and by the drug LY83583, which causes contra

81 boxane A2 (TXA2 ) and prostaglandin F2alpha (PGF2alpha ), on skin microcirculatory blood flow, as wel

82 Thus, prostaglandin F2alpha (PGF2alpha) (FP receptor agonist), Butaprost (EP2 recepto

83 We demonstrate that prostaglandin F2alpha (PGF2alpha) as well as two analogues augment muscle cell

84 For example, prostaglandin F2alpha (PGF2alpha) causes hypertrophy of neonatal rat ventricula

85 type I (AT1R) and the prostaglandin F2alpha (PGF2alpha) F prostanoid (FP) receptors are both potent r

86 Bs in biosynthesis of prostaglandin F2alpha (PGF2alpha) has not been investigated.

87 Prostaglandin F2alpha (PGF2alpha) is a product of cyclooxygenase-catalyzed meta

88 Prostaglandin F2alpha (PGF2alpha) is an important mediator of corpus luteum (CL

89 rogesterone (DHP) and prostaglandin F2alpha (PGF2alpha) levels rise in teleost fish around the time o

90 COX) enzyme product, prostaglandin F2alpha (PGF2alpha), has exhibited promise as an index of oxidant

91 Prostaglandin F2alpha (PGF2alpha), which is released from cells of the myocardi

92 endent relaxations in prostaglandin F2alpha (PGF2alpha)-contracted strips of porcine coronary artery.

93 and the mechanisms of prostaglandin F2alpha (PGF2alpha)-induced protein synthesis in vascular smooth

94 eir endogenous ligand prostaglandin F2alpha (PGF2alpha).

95 classes of isomers of prostaglandin F2alpha (PGF2alpha).

96 pid mediators such as prostaglandin F2alpha (PGF2alpha).

97 -8-iso-PGF2alpha, and prostaglandin-F2alpha (PGF2alpha).

98 se using progesterone, prostaglandin F2alpha(PGF2alpha) and pregnant mare serum gonadotrophin (PMSG).

99 tes mRNA levels of the putative receptor for PGF2alpha (Ptgfr).

100 ated intracellular pathways are required for PGF2alpha to induce morphological and genetic features c

101 lpha, and the isoform NFATC2 is required for PGF2alpha-induced muscle cell growth and nuclear accreti

102 Given this novel role for PGF2alpha in skeletal muscle cell growth, these studies

103 al hydrophobic cavity, thereby preventing FP-PGF2alpha interaction and suppressing the production of

104 PGD2-G, PGF2alpha-G and PGD2-EA, but not PGE2-EA or PGF2alpha-EA

105 in the following order of activity: PGE2-G > PGF2alpha-G > PGD2-G; LYPLA2 hydrolyzed 1- but not 2-ara

106 Although there was no difference in PGF2alpha levels in PVAT between females and males, PGF2

107 ence that the Tnfalpha-dependent increase in PGF2alpha production is necessary for the pro-ovulatory

108 w strategies for therapeutic intervention in PGF2alpha-target tissues.

109 ependent mechanisms appear to be involved in PGF2alpha-induced activation of ERK2; 2) PGF2alpha-induc

110 induced endothelium-dependent relaxations in PGF2alpha-contracted porcine coronary arteries.

111 Here we show that Lh induces PGF2alpha synthesis through its stimulation of Tnfalpha

112 Urinary 8-iso PGF2alpha excretion was associated with the risk of gast

113 Median urinary 8-iso PGF2alpha excretion was higher in cases (0.014; IQR: 0.0

114 Urine 8-iso PGF2alpha was measured primarily by ELISA, and by gas ch

115 , urinary 8-iso prostaglandin F2alpha (8-iso PGF2alpha) as a marker of oxidative stress, and gastric

116 the plasma marker of oxidative stress, 8-iso PGF2alpha, was increased in PHF animals (P < 0.01).

117 Although 12-iso-PGF2alpha caused a dose-dependent activation of the FP,

118 hese observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous desensitization of FP

119 12-iso-PGF2alpha was less potent (EC50 = 5 microM) than PGF2alp

120 o be activated by the F2 isoprostane, 12-iso-PGF2alpha, in addition to its cognate ligand, PGF2alpha.

121 ree radical-catalyzed F2 isoprostane, 12-iso-PGF2alpha, in addition to the cyclooxygenase product, PG

122 In monocyte adhesion assays, 8-iso-PGF2alpha (>10(-8) M) suppressed both basal and TNF-alph

123 r second-trimester levels of 2,3-dinor-8-iso-PGF2alpha (mean change per quartile increase = 0.25, 95%

124 and is highly correlated with urinary 8-iso-PGF2alpha (r = 0.9; P < 0.001).

125 8-Iso-PGF2alpha also had no effect on HMEC surface expression

126 sted, including 8-iso-prostaglandin F (8-iso-PGF2alpha and a purported antagonist (pinane thromboxane

127 er and a strong association of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide with

128 her (p < 0.001) mean values of urinary 8-iso-PGF2alpha and of serum soluble NOX2-derived peptide, ala

129 Urinary 8-iso-PGF2alpha and serum soluble NOX2-derived peptide levels

130 igate any possible correlation between 8-iso-PGF2alpha and the consumption of the two drugs.

131 present study shows the potential for 8-iso-PGF2alpha as a wastewater biomarker for the assessment o

132 iently quantified by this method, with 8-iso-PGF2alpha being identified as a major isomer.

133 The data show that 8-iso-PGF2alpha can suppress the attachment of monocytes to HM

134 as associated with a 4.50% decrease in 8-iso-PGF2alpha concentrations (95% CI: -6.32%, -2.65%) and a

135 The run-in diet reduced 8-iso-PGF2alpha concentrations by 33% (P < 0.0001).

136 Urinary CC16 and 8-iso-PGF2alpha did not increase.

137 Exposure of HMEC to 8-iso-PGF2alpha for 1-2 h was sufficient to reduce monocyte ad

138 Although serum 8-iso-PGF2alpha formation is substantially depressed by COX in

139 8-Iso-PGF2alpha had no effect on the viability (Trypan Blue ex

140 Elevated serum and urine levels of 8-iso-PGF2alpha have been reported in a variety of diseases, m

141 we investigated the potential role of 8-iso-PGF2alpha in inflammation, focusing on its effects on ad

142 he estimated per capita daily loads of 8-iso-PGF2alpha in the 11 cities ranged between 2.5 and 9.9 mg

143 potential anti-inflammatory effect of 8-iso-PGF2alpha in the microvasculature.

144 (CM) transfer experiments suggest that 8-iso-PGF2alpha induces a secondary mediator, which also suppr

145 pha-I, (IPF2alpha-I) a class I isomer (8-iso-PGF2alpha is class IV), using gas chromatography/mass sp

146 The 8-iso-PGF2alpha mass load was found to be strongly associated

147 Although 8-iso-PGF2alpha may be formed as a minor product of COX, this

148 2-iP, iPF2alpha-III (previously called 8-iso-PGF2alpha or 8-epi-PGF2alpha), which demonstrated the ut

149 In contrast, 8-iso-PGF2alpha stimulated monocyte adhesion to human umbilica

150 re patient on hemodialysis and urinary 8-iso-PGF2alpha was 7.1-fold higher in a cigarette smoker than

151 nificant reduction in the excretion of 8-iso-PGF2alpha was induced by the run-in diet and the high-VF

152 20 microCi of tritiated 8-iso-PGF2alpha was infused over 1 h into a male volunteer.

153 The effect of 8-iso-PGF2alpha was mimicked by a thromboxane receptor (TP) ag

154 iet, whereas urinary concentrations of 8-iso-PGF2alpha were further reduced (P < 0.01) by the high-VF

155 In addition, the levels of urinary 8-iso-PGF2alpha were independent predictors of non-alcoholic f

156 The greatest reductions in 8-iso-PGF2alpha were observed in subjects in the highest quart

157 The excretion of 8-iso-PGF2alpha with the low-VF diet remained the same as that

158 One F-ring IsoP, 15-F2t-IsoP (8-iso-PGF2alpha) has been shown to be formed in abundance in v

159 Cell 16 (CC16) and 15-isoprostane F2t (8-iso-PGF2alpha) levels were used to assess lung injury and ov

160 his work, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha) was analysed in raw 24 h-composite wastewater

161 ry excretion of 8-isoprostane F2alpha (8-iso-PGF2alpha) was used as an index of whole-body lipid pero

162 d 8-isoprostane-prostaglandin-F2alpha (8-iso-PGF2alpha), 2,3-dinor-5,6-dihydro-8-iso-PGF2alpha, 2,3-d

163 ma concentrations of F(2)-isoprostane (8-iso-PGF2alpha), 9-hydroxyoctadecadieneoic acid (9-HODE), and

164 the isoprostane 8-iso-prostaglandin F (8-iso-PGF2alpha), among other ligands examined, to activate G1

165 iPF2alpha-III (previously 8-iso-PGF2alpha), an isoprostane from Class III (previously kn

166 ro-15-F2t-IsoP (2,3-dinor-5, 6-dihydro-8-iso-PGF2alpha), by gas chromotography/negative ion chemical

167 produced, 8-iso-prostaglandin F2alpha (8-iso-PGF2alpha).

168 PBDEs were associated with increasing 8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.

169 -iso-PGF2alpha), 2,3-dinor-5,6-dihydro-8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and prostaglandin-

170 Microalbuminuria and urinary 8-iso-PGF2alpha, an index of in vivo oxidative stress, indepen

171 increasing 8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and PGF2alpha.

172 5,6-dihydro-8-iso-PGF2alpha, 2,3-dinor-8-iso-PGF2alpha, and prostaglandin-F2alpha (PGF2alpha).

173 poral trends observed in the levels of 8-iso-PGF2alpha, however, spatial differences were found at th

174 Four additional F2 isoprostanes, 8-iso-PGF2alpha, IPF2alpha-I, IPF2alpha-III, and 9beta,11beta-

175 However, IPF2alpha-I, unlike 8-iso-PGF2alpha, is not formed in a COX-dependent manner by pl

176 assessed by measuring the isoprostane 8-iso-PGF2alpha, was decreased in the lungs of GM-/- mice.

177 eralfold as abundant in human urine as 8-iso-PGF2alpha, with mean values of 737 +/- 20.6 pg/mg creati

178 mplicated p38 and JNK, but not ERK, in 8-iso-PGF2alpha-induced suppression of monocyte adhesion.

179 ct's baseline urinary concentration of 8-iso-PGF2alpha.

180 ng infusion of 500 microg of unlabeled 8-iso-PGF2alpha.

181 quartile of baseline concentrations of 8-iso-PGF2alpha.

182 GF2alpha, in addition to its cognate ligand, PGF2alpha.

183 28767, and misoprostol but not with 10(-6) M PGF2alpha, PGD2, PGI2, or butaprost, suggesting a princi

184 ha levels in PVAT between females and males, PGF2alpha produced a larger contraction in arteries from

185 tor of activated T cells (NFAT) in mediating PGF2alpha-enhanced cell growth was examined.

186 c-fos and identify the diffusable messenger PGF2alpha as obligatory for NMDA receptor-mediated trans

187 ction of intraocular pressure by 50.0 microg PGF2alpha was 5.0+/-1.4 mm Hg, whereas that by 50 microg

188 We show that, within minutes, PGF2alpha injection activates a naturalistic pattern of

189 Moreover, PGF2alpha causes a robust activation ( approximately 50-

190 Twenty-four-hour treatment with 20 nM PGF2alpha, 11-deoxy-PGE1, or PhXA85 reduced the amount o

191 oportion of the ocular hypotensive action of PGF2alpha in cats is mediated by EP1 but not by FP recep

192 y isoprostanes may complement the actions of PGF2alpha in clinical syndromes where oxidant stress and

193 apamycin, implicating mTOR in the actions of PGF2alpha.

194 We conclude that the 22-carbon analogue of PGF2alpha, produced from docosahexaenoic acid by a cyclo

195 To investigate the molecular basis of PGF2alpha receptor (FP) activation in the eye, we cloned

196 When the concentration of PGF2alpha, 11-deoxy-PGE1, or PhXA85 was increased to 200

197 ent administration of 12.5 microg of each of PGF2alpha and 17-phenyl trinor PGE2 did not produce an a

198 The biological effects of PGF2alpha are mediated via the G protein-coupled recepto

199 The effects of PGF2alpha were mimicked by the PKC activator PMA and inh

200 t metacyclic stage, as did the expression of PGF2alpha synthase (PGFS).

201 se relationship exists between the levels of PGF2alpha and a steroid-inducible anti-inflammatory prot

202 Levels of PGF2alpha and thromboxane B2 (TXB2 ) were quantified by

203 ty by PD 098059 led to a significant loss of PGF2alpha-induced eIF4E and 4E-BP1 phosphorylation, glob

204 med that COX-1 accounted for the majority of PGF2alpha production.

205 Following the removal of PGF2alpha, however, FPA-expressing cells return to their

206 e-dependent manner while having no effect on PGF2alpha-stimulated inositol phosphates formation.

207 Only PGF2alpha up-regulated CTGF mRNA expression in the cat i

208 Consistent with these observations, only PGF2alpha and 12-iso-PGF2alpha caused rapid homologous d

209 PGF2alpha-G and PGD2-EA, but not PGE2-EA or PGF2alpha-EA, also increased the frequency of mIPSCs.

210 er PGT nor PG15DH, exogenously added PGE2 or PGF2alpha were rapidly oxidized to the 13, 14-dihydro, 1

211 catalyzed the transport of PGE1, PGE2, PGD2, PGF2alpha, and, to a lesser degree, TXB2.

212 because unreactive lipids, e.g. PGB1, PGE2, PGF2alpha, and TxB2, did not inhibit LKB1 activity (p >

213 nhibitor of p70(S6k), also failed to prevent PGF2alpha-induced global protein synthesis and bFGF-2 ex

214 , in addition to the cyclooxygenase product, PGF2alpha.

215 synthesis of the most complex prostaglandin, PGF2alpha, with high levels of control of relative and a

216 The potency of the natural prostaglandins PGF2alpha and PGD2 was not enhanced by the mutations.

217 triggers the synthesis of the prostaglandins PGF2alpha and PGE2, but not PGD2, in rat cerebral cortic

218 Recently, PGF2alpha analogs have been hypothesized to reduce intra

219 n by binding and most likely by sequestering PGF2alpha into its central hydrophobic cavity, thereby p

220 Similarly, PGF2alpha causes translocation of cytosolic phospholipas

221 Similarly, PGF2alpha-mediated vasoconstriction was symmetrically re

222 , induced mkp1 mRNA to a greater extent than PGF2alpha and fluprostenol, which activate PKC signaling

223 alpha was less potent (EC50 = 5 microM) than PGF2alpha (EC50 = 10 nM) in generating inositol phosphat

224 Additional studies demonstrate that PGF2alpha stimulates protein tyrosine phosphorylation an

225 We demonstrate that PGF2alpha treatment results in a timeand concentration-d

226 We further demonstrate that PGF2alpha, but not PGE2 or PGD2, is necessary but not su

227 minant-interfering proteins demonstrate that PGF2alpha-induced myocyte hypertrophy occurs independent

228 It is established that PGF2alpha binds to a G-proteincoupled receptor (GPCR) to

229 It was also found that PGF2alpha-could activate T-cell factor (Tcf)/beta-cateni

230 ne chip technology, we first identified that PGF2alpha dramatically up-regulated Cyr61 and CTGF mRNA

231 c ring contraction experiments revealed that PGF2alpha-dependent activation of FP potentiated angiote

232 vely, whereas neither compound abrogates the PGF2alpha-mediated response.

233 This growth is mediated through the PGF2alpha receptor (FP receptor).

234 f neonatal rat ventricular myocytes, via the PGF2alpha receptor (FP).

235 Therefore, PGF2alpha and Bimatoprost appear to interact with differ

236 Thus, PGF2alpha and 8,12-iso-iPF2alpha-III stimulate inositol

237 contained F-type prostane rings analogous to PGF2alpha.

238 This increased myotube size is not due to PGF2alpha-enhancing cell fusion that initially forms myo

239 roxylamine (HA, 100 mum), altered the NPV to PGF2alpha (BCA increased, HA inhibited) and/or LY83583 (

240 that initially forms myotubes, but rather to PGF2alpha recruiting the fusion of cells with preexistin

241 suggest that GPCR activation in response to PGF2alpha stimulates the mTOR pathway which increases th

242 The stimulation of S6K1 in response to PGF2alpha treatment was abolished by the mTOR inhibitor

243 respectively) on the intraocular response to PGF2alpha were also examined.

244 9220 on the intraocular pressure response to PGF2alpha.

245 effect on the ocular hypotensive response to PGF2alpha.

246 nsignificant effect on the pupil response to PGF2alpha.

247 s mediate hypertrophic growth in response to PGF2alpha.

248 intraocular pressure and pupil responses to PGF2alpha, are mediated by EP1 and FP receptors, respect

249 om female animals and greater sensitivity to PGF2alpha in the porcine coronary artery from males.

250 (TxS), and the receptors for TxA2 (the TP), PGF2alpha (the FP), and PGI2 (the IP) were upregulated a

251 anges in c-Jun-dependent gene transcription, PGF2alpha preferentially activates the MEK-Erk2- cytosol

252 trictor responses to norepinephrine, U46619, PGF2alpha, vasopressin, BAY K8644; biphasic responses to

253 In the dose ranges used, PGF2alpha and 17-phenyl trinor PGE2 decreased intraocula

254 sed the ability of 8-isoPGF2alpha, 5iPF2 VI, PGF2alpha, and a mixture containing these PGs in a 0.5/0

255 The rank order substrate profile was PGF2alpha approximately PGE2 > TXB2 >> 6 keto-PGF1alpha.

256 ontraction in arteries from females, whereas PGF2alpha appears to mediate the contraction in arteries

257 eriments were performed to determine whether PGF2alpha stimulates the mammalian target of rapamycin (

258 ar sex differences in PVAT function in which PGF2alpha and TXA2 antagonists can inhibit the PVAT-indu

259 indings are consistent with a model in which PGF2alpha communicates fertility status via Ptgfr to cir

260 GE2 has much lower efficacy as compared with PGF2alpha for the activation of Tcf/beta-catenin signali

261 lon to the myocyte membrane, consistent with PGF2alpha receptor coupling to Gq.

262 ependent p70(S6k) activation correlates with PGF2alpha-induced global protein synthesis and bFGF-2 ex

263 d also exhibited cross-desensitization, with PGF2alpha resulting in a maximum of approximately 60% de

264 in monolayer cultures and were treated with PGF2alpha, 11-deoxy-PGE1, or PhXA85 (the nonesterified a

265 Treatment with PGF2alpha did not increase AKT phosphorylation but incre

266 iated cell rounding following treatment with PGF2alpha.