ライフサイエンスコーパス: AEA

1 AEA acts as an endocannabinoid and an endovanilloid by a

2 AEA analysis was linear over the range 0.23 to 19 nM (1.

3 AEA caused a significant decrease in cell number only at

4 AEA concentrations were significantly negatively correla

5 AEA has been isolated from numerous tissues and biofluid

6 AEA hydrolysis was detectable at the earliest measurable

7 AEA is hydrolyzed by fatty acid amide hydrolase (FAAH),

8 AEA significantly inhibited cytokine production from hea

9 AEA uptake and hydrolysis were significantly potentiated

10 AEA was analyzed in cord and maternal blood, amniotic fl

11 AEA was detected in serum and plasma from blood isolated

12 AEA was found to induce a preferential processing of Not

13 AEA was readily trafficked to lipid droplets, confirming

14 AEA was undetectable in saliva and urine.

15 AEA-treated keratinocytes showed reduced an induction of

16 2 knockdown in dCAD cells did not affect [3H]AEA uptake.

17 increase in the overall levels of intact [3H]AEA associated with the cells, suggesting that trafficki

18 he cells, suggesting that trafficking of [3H]AEA to FAAH had been disrupted.

19 Results using the [(2)H(4)]AEA and HPLC-MS/MS method agreed well with those obtaine

20 eukocyte assay using stably labeled [(2)H(4)]AEA as substrate.

21 The 60% AEA extraction efficiency achieved with SPE from plasma

22 ous studies have mapped anti-erythrocyte Ab (AEA)-promoting NZB loci to several chromosomal locations

23 validated method using octa-deuterated AEA (AEA-d8) as an internal standard represents an improvemen

24 differentially modulates brain lipid (2-AG, AEA, and OEA) signaling, and these modulations are influ

25 2-AG, AEA, and WIN55,212-2, enhanced Galpha(i/o) and Gbetagamm

26 2-AG, AEA, THC, and WIN55,212-2 also activated Galpha(q)-depen

27 e alpha2 subunit converted the alpha1/alpha3 AEA-sensitive receptors to sensitivity resembling that o

28 Although AEA and 2-AG likely subserve distinct physiological role

29 k suggests that rapid reductions in amygdala AEA signaling following stress may prime the amygdala an

30 s the existence and the activity of FAAH, an AEA-metabolizing enzyme, in the TM tissues.

31 , we develop Annotation Enrichment Analysis (AEA), which properly accounts for the non-uniformity of

32 Anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are the most char

33 Anandamide (AEA) and other bioactive N-acylethanolamines (NAEs) are

34 Anandamide (AEA) content was downregulated after repeated seizures,

35 Anandamide (AEA) is an endogenous intestinal cannabinoid that contro

36 Anandamide (AEA) is an endogenous ligand of cannabinoid receptors an

37 h 2-arachidonoylglycerol (2-AG), anandamide (AEA), CP55,940, Delta(9)-tetrahydrocannabinol (THC), can

38 ndogenous CB1 receptor agonists, anandamide (AEA), increases during development in whole-brain sample

39 -arachidonoylglycerol (2-AG) and anandamide (AEA) activate a canonical cannabinoid receptor in Caenor

40 -arachidonyl glycerol (2-AG) and anandamide (AEA)), two synthetic cannabinoids (WIN55,212-2 and CP55,

41 iny neurons (MSNs) with the eCBs anandamide (AEA) or 2-arachidonoylglycerol and determined the condit

42 We show that the endocannabinoid anandamide (AEA) can alter neuronal cell function both through its e

43 we show that the endocannabinoid anandamide (AEA) is a key mediator of hypoxic pulmonary vasoconstric

44 H), which alters endocannabinoid anandamide (AEA) levels, would impact the development of frontolimbi

45 ar uptake of the endocannabinoid anandamide (AEA) occurs has been the source of much debate.

46 ubation with the endocannabinoid anandamide (AEA) substantially increased the amplitude of glycine-ac

47 he levels of the endocannabinoid anandamide (AEA) when administered to humans, suggesting that phytoc

48 reduction in the endocannabinoid anandamide (AEA), within the amygdala.

49 sporters for the endocannabinoid anandamide (AEA).

50 trations of the endocannabinoid, anandamide (AEA), in both their plasma and their endometrial tissue

51 ect of the main endocannabinoid, anandamide (AEA), in these DC subsets and correlated cytokine levels

52 ned whether the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are released by

53 e the two major endocannabinoids anandamide (AEA) and 2-arachidonoylglycerol (2-AG), respectively, ha

54 trations of the endocannabinoids anandamide (AEA) and 2-arachidonylglycerol (2-AG) with brain functio

55 f levels of the endocannabinoids anandamide (AEA) or 2-arachidonoylglycerol (2-AG) in the rACC follow

56 cells secrete endocannabinoids, anandamide (AEA) (35 pg/10(7) cells), and 2-AG (75.2 ng/10(7) cells)

57 The two endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), play independent

58 fluence of the endocannabinoids, anandamide (AEA) and 2-arachidonoylglycerol, on the Notch-1 pathway

59 ermine the effects of endogenous anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) on the permeabil

60 s signaling lipids that includes anandamide (AEA).

61 mal melanocyte cells), including anandamide (AEA), 2-arachidonoylglycerol, the respective target rece

62 atty acid amides (FAA) including anandamide (AEA), palmitoylethanolamide (PEA), and N-oleoylethanolam

63 ces neurodegeneration, increased anandamide (AEA) but not 2-arachidonylglycerol biosynthesis and CB1R

64 ne-naive controls, and increased anandamide (AEA) release during nicotine intake.

65 Increased anandamide (AEA) signaling through inhibition of its catabolic enzym

66 CB2), their endogenous ligands, anandamide (AEA) and 2-arachidonoylglycerol, and metabolic enzymes o

67 hanges in the two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), with stress exp

68 e research on the trafficking of anandamide (AEA) across cell membranes, little is known about the me

69 the anti-hyperalgesic effects of anandamide (AEA) and cyclohexylcarbamic acid 3'-carbamoyl-biphenyl-3

70 AAH) produces elevated levels of anandamide (AEA) and promotes fear extinction, suggesting that FAAH

71 with a decrease in the level of anandamide (AEA) in plantar paw skin ipsilateral to tumors.

72 was accompanied by a decrease of anandamide (AEA) levels in the amygdala and prefrontal cortex, and t

73 inoid (eCB) system, particularly anandamide (AEA) signaling, controls neuronal excitability and seizu

74 lular CB1R-dependent signalling, anandamide (AEA) has come to the forefront in several novel contexts

75 ging evidence has suggested that anandamide (AEA), an endogenous agonist of cannabinoid (CB) receptor

76 JZL184 (0.1-1 mug/side), and the anandamide (AEA) hydrolysis inhibitor URB597 (10-30 ng/side) were ad

77 2-arachidonylglycerol [2-AG] and anandamide [AEA]) in 3T3-L1 adipocytes.

78 aling, we measured the amount of anandamide [AEA (N-arachidonoylethanolamine)] and 2-arachidonoylglyc

79 modulated by the endocannabinoid anandamide(AEA) and its receptors: cannabinoid-1 (CB1), cannabinoid

80 2-AG and AEA displayed Galphai/o/Gbetagamma bias and normalized C

81 i/o) and Gbetagamma signaling, with 2-AG and AEA treatment leading to increased total CB1 levels.

82 increased plasma EC concentrations (2-AG and AEA) and elevated adipose tissue 2-AG.

83 f acute stress to modulate amygdala FAAH and AEA in both rats and mice is also mediated through CRHR1

84 jor psychoactive component of marijuana, and AEA.

85 anandamide [i.e., arachidonoylethanolamide (AEA)] has been attributed to reduced activity of the AEA

86 ess also reduced N-arachidonoylethanolamine (AEA), an endogenous ligand of CB(1)R.

87 sts CP55,940 and N-arachidonoylethanolamine (AEA).

88 N-Arachidonoylethanolamine (AEA, anandamide) was the first endocannabinoid to be ide

89 Anandamide (N-arachidonoylethanolamine, AEA) is an endocannabinoid present in human plasma that

90 noid anandamide (N-arachidonoylethanolamine, AEA).

91 abinoid anandamide (arachidonylethanolamide, AEA) on the function of alpha4beta2 nicotinic acetylchol

92 ration of the eCB N-arachidonylethanolamine (AEA) within the amygdala.

93 d via anandamide (N-arachidonylethanolamine [AEA]) and 2-arachidonoylglycerol (2-AG) in the regulatio

94 ecule capsaicin (CP) has a similar effect as AEA; however, CP acts by engagement of the vanilloid rec

95 Consistent with the roles of FABP as AEA carriers, administration of the competitive FABP lig

96 on-lipid FABP inhibitor BMS309403 attenuated AEA uptake and hydrolysis by approximately 50% in N18TG2

97 e dependently associated with elevated basal AEA levels, facilitated fear extinction, and enhanced th

98 sulting from a positive association of basal AEA concentrations and putamen activity to rewarding sti

99 Because AEA and 2-AG undergo rapid and almost complete intracell

100 otentially wider therapeutic overlap between AEA and 2-AG augmentation approaches than was previously

101 nxiety and the functional redundancy between AEA and 2-AG signaling in the modulation of anxiety-like

102 Boosting AEA signaling through inhibition of its degradative enzy

103 Both CB(1) (by AEA and 2-AG) and non-CB(1) (by OEA) targets can alter t

104 atinocytes, and found that CB1 activation by AEA suppressed production and release of signature TH1-

105 ly emphasized when ECS was hyperactivated by AEA and in ob/ob tissue.

106 ibited the potentiation of I(Gly) induced by AEA and THC.

107 onsiveness to cytokine inhibition induced by AEA.

108 n the enhanced Notch-1 signaling mediated by AEA.

109 Notch-1, numb (Nb), this can be prevented by AEA and 2-arachidonoylglycerol.

110 The inhibition of 5-HT(3) receptors by AEA may contribute to its physiological roles in control

111 , arachidonoyl-[1-(14)C]ethanolamide ([(14)C]AEA) uptake, and FABP knockdown to demonstrate that tran

112 (5 mum), a functional synergism on cellular AEA and 2-AG uptake was observed.

113 l membrane transporter controls the cellular AEA and 2-AG trafficking and metabolism.

114 unt for the observed increase in circulating AEA in humans following CBD consumption.

115 These results show that circulating AEA may modulate brain activation during reward feedback

116 We also show that at higher concentrations AEA induces normal human epidermal melanocyte apoptosis

117 However, at lower concentrations, AEA and other CB(1)-binding endocannabinoids dose-depend

118 Interestingly, depleting AEA signaling in the BLA did not prevent fear conditioni

119 s efficacious in potentiating I(Gly), desoxy-AEA inhibited potentiation produced by both Delta(9)-tet

120 While desoxy-AEA was significantly less efficacious in potentiating I

121 fully validated method using octa-deuterated AEA (AEA-d8) as an internal standard represents an impro

122 to the anti-hyperalgesic effect of elevated AEA levels.

123 and that loss of this tone through elevated AEA hydrolysis increases inhibition in the BLA, which in

124 alpha4beta2 nAChR function by an endogenous AEA-like lipid.

125 e results of this study show that endogenous AEA and 2-AG production and CB1 activation play a key mo

126 940 to the CB1 receptor as well as enhancing AEA-stimulated [(35)S]GTPgammaS binding in mouse brain m

127 endocannabinoids, arachidonyl ethanolamide (AEA) and 2-arachidonylglycerol (2-AG), to prostaglandin-

128 inoid anandamide (arachidonoyl ethanolamide, AEA) is an uncharged neuromodulatory lipid that, similar

129 Our aims were to (1) evaluate AEA levels at the human maternal:fetal interface and (2)

130 However, to pharmacologically exploit AEA and/or 2-AG signaling in this way, we must first gai

131 trol, loss > control) and concentrations for AEA and 2-AG as factors.

132 Regression analyses were conducted for AEA and 2-AG on TPQ-RD scores.

133 Analyzing the fMRI data, for AEA and 2-AG ANCOVAs were calculated using a full factor

134 Limits of quantification and detection for AEA were also improved dramatically using SPE (8 and 4 f

135 fficient cytosolic trafficking mechanism for AEA.

136 tal issues such as the synthesis pathway for AEA and the molecular mechanism(s) underlying cellular u

137 Here, we uncover a role for AEA and its receptor, cannabinoid receptor 2 (CB2), in t

138 for tissues spiked with 0.2, 1, and 5pmol/g AEA of less than 12%.

139 y for fatty acid ethanolamide ligands (e.g., AEA) evolved thereafter.

140 eed well with those obtained using the [(3)H]AEA radiometric assay.

141 at leukocyte FAAH activity assay using [(3)H]AEA, we have developed a human leukocyte assay using sta

142 Postmenopausal women had AEA concentrations comparable to levels observed during

143 ediating the HFD-induced increase in hepatic AEA, which then activates hepatic CB1R to induce insulin

144 e we show that HFD-induced increased hepatic AEA levels and decreased FAAH activity are absent in SCD

145 of hepatic FAAH activity, normalizes hepatic AEA levels, and improves insulin sensitivity.

146 nt cancer cell lines die in response to high AEA concentrations.

147 Higher AEA concentrations were found in placenta compared to fe

148 However, AEA accelerated 5-HT(3A) receptor desensitization time i

149 omogenate activity assays, FAAH-2 hydrolyzed AEA and palmitoylethanolamide (PEA) with activities appr

150 In contrast, FAAH-2 hydrolyzed AEA and PEA in intact cells with rates approximately 30-

151 onist, arachidonic acid N-hydroxyethylamide (AEA), indicating the effectiveness of treatments in modu

152 ivity in the VTA, suggesting that changes in AEA and OEA signaling result from alterations in their n

153 The relevance of these changes in AEA concentrations at the maternal:fetal interface requi

154 re sufficient to evoke phenotypic changes in AEA signaling in DRG neurons.

155 tudies have demonstrated that the decline in AEA appears to contribute to the manifestation of the st

156 The decrease in AEA occurred in conjunction with increased degradation o

157 rotected against stress-induced decreases in AEA and negative emotional consequences of stress.

158 ies indicate that FAAH-mediated decreases in AEA occur following chronic stress and that this loss of

159 rotected against stress-induced decreases in AEA, both in the periphery, and also in the amygdala and

160 odel to evaluate the impact of elevations in AEA signaling in humans, helping to inform whether FAAH

161 ty blocked the training-induced increases in AEA levels as well as the memory enhancement produced by

162 strated the involvement of these proteins in AEA-induced melanogenesis.

163 Significant variability in AEA plasma concentrations has been reported between stud

164 congenic mice exhibited marked reductions in AEAs and splenomegaly but not in anti-nuclear Abs.

165 res with the FAAH inhibitor URB597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive mann

166 Inhibition of FAAH activity increases AEA concentrations in nervous tissue and reduces sensory

167 nhibitor URB597, which selectively increases AEA levels at active synapses, administered into the bas

168 that emotionally arousing training increases AEA levels within prefrontal-limbic circuits and strongl

169 s the source responsible for hypoxia-induced AEA generation.

170 Interestingly, AEA up-regulated Nct expression, a component of gamma-se

171 rain were examined as possible intracellular AEA carriers.

172 increases in anxiety associated with limbic AEA deficiency.

173 Mean AEA concentrations were 2.72 + or - 1.04 pmol/g for plac

174 ay variability were comparable, and the mean AEA concentration of pooled plasma samples (1.18 nM, n=1

175 BPs) are intracellular proteins that mediate AEA transport to its catabolic enzyme fatty acid amide h

176 Moreover, AEA signaling augmentation also rescued the seizure-indu

177 B597, an FAAH inhibitor, the effect of 10 nM AEA on outflow facility was prolonged by at least 4 hour

178 In human U937 leukemia cells, 100 nm AEA and 1 mum 2-AG were taken up through a fast and satu

179 yed an increase in hippocampal 2-AG, but not AEA, levels at the time of retention testing and a decre

180 Accumulation of AEA and 2-AG was achieved by inhibiting their metabolizi

181 P5 in mice results in excess accumulation of AEA, abolishes PPARbeta/delta activation in the brain, a

182 The actions of AEA were apparent when applied extracellularly but not d

183 activity studies, the enzymatic activity of AEA hydrolysis was detected in TM tissues, and this acti

184 t to rimonabant,the I.C.V. administration of AEA (50 mug) enhanced LPS hypothermia.

185 Administration of AEA caused a transient enhancement of aqueous humor outf

186 study demonstrate that the administration of AEA increases aqueous humor outflow facility and that th

187 rons) to determine whether administration of AEA results in abnormal responses of group IV afferent n

188 Further, oral administration of AEA to NOD mice provides protection from T1D.

189 of biomatrices containing limited amounts of AEA.

190 Further analysis of AEA effects on alpha4beta2 nAChR-mediated currents, usin

191 this method is suitable for the analysis of AEA in clinical samples and may be utilised for the inve

192 method is described here for the analysis of AEA in human plasma.

193 by selective pharmacological augmentation of AEA signaling and via direct cannabinoid receptor 1 stim

194 nhibit the cellular uptake and catabolism of AEA by targeting FABPs.

195 s were collected for plasma concentration of AEA, PEA, OEA, and JNJ-42165279.

196 Basal concentrations of AEA and 2-AG were determined in serum.

197 in conjunction with increased degradation of AEA by fatty acid amide hydrolase (FAAH).

198 sional barrier for the efficient delivery of AEA to its site of catabolism.

199 s showed a significant interaction effect of AEA concentration by condition (positive vs. negative) w

200 sclose a distinct immunomodulatory effect of AEA in mDCs and pDCs from MS patients, which may reflect

201 mor outflow facility and that this effect of AEA involves CB1 and CB2 cannabinoid receptors.

202 by the prominent vasoconstrictive effect of AEA on pulmonary arteries and strongly reduced HPV in FA

203 The effect of AEA was measured at different timepoints (4, 18, 24, 48,

204 Furthermore, the effects of AEA ACh currents were not altered by the calcium chelato

205 oreactivity as well as inhibitory effects of AEA and URB597 on the depolarization-evoked Ca(2+) trans

206 mportantly, the anti-hyperalgesic effects of AEA and URB597 were blocked by a CB1 receptor antagonist

207 The effects of AEA could be neither replicated by the exogenous cannabi

208 The effects of AEA on aqueous humor outflow were measured using a porci

209 The stimulatory effects of AEA on Notch-1 signaling persisted in the presence of Ab

210 We aimed to investigate the effects of AEA on the survival and proliferation of an endometrial

211 seizures, and pharmacological enhancement of AEA signaling rescued seizure-induced anxiety by restori

212 a robust SPE technique for the extraction of AEA from biomatrices to replace the existing liquid extr

213 alidate the use of solid-phase extraction of AEA from tissues.

214 suggest that pharmacological facilitation of AEA signaling is a promising strategy for attenuating ci

215 FABP5 both promotes the hydrolysis of AEA into arachidonic acid and thus reduces brain endocan

216 ry measurements revealed a clear increase of AEA and the FAAH-dependent metabolite arachidonic acid i

217 iphenyl-3-yl ester (URB597), an inhibitor of AEA hydrolysis.

218 Intraplantar injection of AEA (10 mug/10 mul) or URB597 (9 mug/10 mul) transiently

219 lar responses to intra-arterial injection of AEA into the hindlimb of normal, cardiomyopathic and neo

220 Intraplantar injection of AEA reduced the hyperalgesia, and intraplantar injection

221 action (SPE) method for the investigation of AEA concentrations in human plasma, serum, milk, urine,

222 ibitor of FAAH, increased the local level of AEA and also reduced hyperalgesia.

223 re accompanied by a decrease in the level of AEA in plantar paw skin.

224 lipopolysaccharide (LPS), elevated levels of AEA (75.6 pg/10(7) cells) and 2-AG (98.8 ng/10(7) cells)

225 shock intensity produced increased levels of AEA in the amygdala, hippocampus, and medial prefrontal

226 id 1 receptor density or change in levels of AEA or 2-AG.

227 a pronounced increase in striatal levels of AEA, but not the other major endogenous cannabinoid 2-ar

228 AH)(-/-) mice, which have elevated levels of AEA, yielded increased colony formation as compared with

229 llowing chronic stress and that this loss of AEA signaling is functionally relevant to the effects of

230 urface receptor expression, the magnitude of AEA inhibition decreased.

231 The magnitude of AEA inhibition was inversely correlated with the express

232 tamine (5-HT) and increased the magnitude of AEA inhibition.

233 desensitization and reduced the magnitude of AEA inhibition.

234 The magnitude of AEA potentiation decreased with removal of either the hy

235 eizures cause an allostatic maladaptation of AEA signaling in the amygdala that drives emotional alte

236 Pharmacological manipulation of AEA and 2-AG signaling should prove to have significant

237 ulness of this method for the measurement of AEA levels in clinical samples, plasma samples obtained

238 out the molecular and cellular mechanisms of AEA-induced direct effects on LGICs.

239 These results indicate that modulation of AEA signaling represents a potential and promising targe

240 OMDM-2 inhibit the bidirectional movement of AEA and 2-AG across cell membranes.

241 desensitization kinetics and the potency of AEA-induced inhibiting effect on the receptors.

242 esults directly demonstrated the presence of AEA-specific promoting genes on NZB chromosome 4, docume

243 receptor TRPV1, causing local production of AEA, which acts through CB2.

244 d between studies, because quantification of AEA is fraught with methodological difficulties.

245 cells were cultured in vitro, and a range of AEA concentrations (0-10 000 nM) were added to the cells

246 ibitors also blocked the cellular release of AEA and 2-AG.

247 However, examining the role of AEA signaling in stress, anxiety, and fear through pharm

248 The substrate specificity of AEA compared to those of PG-Gs was approximately 200-300

249 nd events responsible for the termination of AEA and 2-AG signaling.

250 l of either the hydroxyl or oxygen groups on AEA.

251 mice showed that the full effect of Lbw2 on AEA production was dependent on three subloci, with sple

252 2-AG or AEA activate NPR-19 directly and cannabinoid-dependent i

253 2-AG or AEA inhibit nociception and feeding through a pathway re

254 urified MGL and FAAH compared to 2-AG and/or AEA.

255 Our data suggest that a permissive AEA tone within the BLA might gate GABA release and that

256 Plasma AEA concentrations were significantly (P=0.0078) lower i

257 The highest plasma AEA levels were observed in women in active labour, and

258 To study this process, AEA uptake and hydrolysis were examined in COS-7 cells e

259 of fatty acid amide hydrolase (FAAH) reduces AEA, we confirmed that oral administration of an FAAH in

260 ycerol (2-AG), with stress exposure reducing AEA levels and increasing 2-AG levels.

261 ngly suggests that the endogenously released AEA modulates memory consolidation.

262 he robust developmental increase in striatal AEA may be the key factor in the emergence of HFS-induce

263 In summary, AEA has the proclivity to enhance Notch-1 signaling in a

264 the BLA to assess the impact of suppressing AEA signaling on stress, fear, and anxiety in male rats.

265 Furthermore, application of synthetic AEA during HFS in field recordings of slices from P12-P1

266 and were significantly (P=0.0389) lower than AEA plasma concentrations obtained during the follicular

267 en together, these findings demonstrate that AEA suppresses highly pathogenic T cell subsets through

268 We determined that AEA controls changes in blood pressure, predominately vi

269 These data indicate that AEA and 2-AG signaling pathways interact to regulate spe

270 These results indicate that AEA directly inhibits the function of alpha4beta2 nAChRs

271 Taken together, these findings indicate that AEA-mediated activation of CB(1) receptors is crucial fo

272 s not treated with LPS, thus indicating that AEA modulates LPS-activated pathways in the brain rather

273 Here, we report that AEA inhibited the function of serotoningated ion channel

274 We report that AEA up-regulates Notch-1 signaling in cultured neurons.

275 Our results show that AEA induces a decrease in Ishikawa cell number probably

276 We show that AEA is able to identify biologically meaningful function

277 Collectively, these data suggest that AEA signaling can temper aspects of the stress response

278 The AEA-induced enhancement of outflow facility was blocked

279 The AEA/CB1R/pERK1/2 signaling pathway may be directly respo

280 bohydrate and lipid metabolism, blunting the AEA-induced increase in gene expression of proteins rela

281 d nearly 30-fold as a linear function of the AEA concentration.

282 The onset and washout of the AEA effects required several minutes (10-30 min), but th

283 ith hydrolase-inactive concentrations of the AEA transport inhibitors UCM707 (1 mum) and OMDM-2 (5 mu

284 s been attributed to reduced activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH).

285 restored at 48 and 72 h suggesting that the AEA growth inhibitory effect is time limiting.

286 Thus, the AEA/FAAH pathway is an important mediator of HPV and is

287 desensitization time was correlated with the AEA-induced inhibiting effect and mean 5-HT current dens

288 Therefore, AEA likely traverses the cytosol with the assistance of

289 Tissue AEA was quantified using an isotope-dilution method and

290 suggest that the increased plasma and tissue AEA concentrations observed in patients with endometrial

291 alpha2 subunit was relatively insensitive to AEA.

292 and alpha3 subunits were highly sensitive to AEA-induced potentiation, the alpha2 subunit was relativ

293 Ishikawa cells were sensitive to AEA-mediated cytotoxicity in a pseudo dose-dependent man

294 signaling coordinates a disruption of tonic AEA activity to promote a state of anxiety, which in tur

295 resent the first proteins known to transport AEA from the plasma membrane to FAAH for inactivation an

296 Intriguingly, structurally unrelated AEA uptake inhibitors also blocked the cellular release

297 ted behavior by postnatal day 45 (P45), when AEA levels begin to decrease, and also, at P75 but not b

298 e, Ishikawa, contains the receptors to which AEA binds.

299 measure reward dependence is correlated with AEA concentrations in healthy human volunteers.

300 r N-acylethanolamines did not interfere with AEA and 2-AG uptake.