ライフサイエンスコーパス: fatty acid amide

1 tion to FAAH that could hydrolyze long-chain fatty acid amides.

2 molecules collectively known as the primary fatty acid amides.

3 class of endogenous signaling lipids termed fatty acid amides.

4 tified in Stevia for the first time, such as fatty acid amides.

5 the main enzyme catabolizing endocannabinoid fatty acid amides.

6 amily of bioactive signalling molecules, the fatty-acid amides.

7 lead to additional insights into the role of fatty acid amide activity in human biological systems an

8 5 eCBs and related compounds, including both fatty acid amides and glycerols.

9 Primary fatty acid amides are a group of bioactive lipids that h

10 osynthesis, and its proposed role in primary fatty acid amide biosynthesis has been controversial.

11 at these proteins may collaborate to control fatty acid amide catabolism in primates.

12 n lowering plasma total cholesterol than the fatty acid amide CI-976.

13 The most prevalent elicitors are fatty acid amides consisting of 18-carbon polyunsaturate

14 Fatty acid amides constitute a large and diverse class o

15 Therefore, formulating the long-chain fatty acid amide derivatives of nucleoside analogs into

16 No appreciable amounts of fatty acid amides (e.g., oleamide), ceramides, or monoac

17 her elicitors including volicitin, the first fatty acid amide elicitor identified in caterpillars.

18 ATP-independent in vitro biosynthesis of the fatty acid amide elicitor, N-linolenoyl-l-glutamine, by

19 Fatty acid amides (FAAs) constitute a large class of end

20 finding of oleamide and other members of the fatty acid amide family in the tear film could lead to a

21 n integral membrane enzyme that degrades the fatty acid amide family of endogenous signaling lipids,

22 n integral membrane enzyme that degrades the fatty acid amide family of signaling lipids, including t

23 is the best-understood member of the primary fatty acid amide family.

24 Fatty acid amide hydrolase (EC 3.5.1.4.) is the enzyme r

25 Here we show that mice lacking the enzyme fatty acid amide hydrolase (FAAH(-/-)) are severely impa

26 ates a common human mutation in the gene for fatty acid amide hydrolase (FAAH) (C385A; rs324420), the

27 aint stress, which results in an increase in fatty acid amide hydrolase (FAAH) activity and a reducti

28 Fatty acid amide hydrolase (FAAH) activity in mammals ha

29 A decrease in fatty acid amide hydrolase (FAAH) activity increases the

30 el fluorescent assay to continuously monitor fatty acid amide hydrolase (FAAH) activity that is simpl

31 cells, and then anandamide is hydrolyzed by fatty acid amide hydrolase (FAAH) and 2-AG by monoacylgl

32 paradigm to exert combined activity at human fatty acid amide hydrolase (FAAH) and dopamine receptor

33 rotein that may modulate CB(1) function; and fatty acid amide hydrolase (FAAH) and N-acylethanolamine

34 hibitors 3-5 bound to a humanized variant of fatty acid amide hydrolase (FAAH) are disclosed and comp

35 Monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH) are two enzymes from t

36 c enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydrolase (FAAH) attenuates naloxone-pr

37 Inhibition of the enzyme fatty acid amide hydrolase (FAAH) counteracts reward-rel

38 Fatty acid amide hydrolase (FAAH) degrades NAE into etha

39 Fatty acid amide hydrolase (FAAH) degrades neuromodulati

40 Fatty acid amide hydrolase (FAAH) degrades the endocanna

41 Measuring uptake at 25 s, when fatty acid amide hydrolase (FAAH) does not appreciably a

42 dized by lipoxygenase (LOX) or hydrolyzed by fatty acid amide hydrolase (FAAH) during normal seedling

43 In this report, we isolated the enzyme fatty acid amide hydrolase (FAAH) from mouse serum as an

44 he action of diverse hydrolases, among which fatty acid amide hydrolase (FAAH) has been well characte

45 The integral membrane enzyme fatty acid amide hydrolase (FAAH) hydrolyzes the endocan

46 tigated the role of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH) in AEA-induced cell de

47 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o

48 holipase D (NAPE-PLD) and its degradation by fatty acid amide hydrolase (FAAH) in mouse embryos and o

49 ain lipids regulated by the mammalian enzyme fatty acid amide hydrolase (FAAH) in vivo, including kno

50 lly mediated by the integral membrane enzyme fatty acid amide hydrolase (FAAH) in vivo.

51 Fatty acid amide hydrolase (FAAH) inactivates a large an

52 Fatty acid amide hydrolase (FAAH) inactivates the endoge

53 A recent phase 1 trial of the fatty acid amide hydrolase (FAAH) inhibitor BIA 10-2474

54 We found that both the fatty acid amide hydrolase (FAAH) inhibitor URB597 and t

55 l finding that posttraining infusions of the fatty acid amide hydrolase (FAAH) inhibitor URB597, whic

56 The peripherally restricted fatty acid amide hydrolase (FAAH) inhibitor URB937 (3, c

57 ntified benzothiazole analogue 3 as a potent fatty acid amide hydrolase (FAAH) inhibitor.

58 nd characterization of alpha-ketoheterocycle fatty acid amide hydrolase (FAAH) inhibitors are disclos

59 nd urea derivatives are important classes of fatty acid amide hydrolase (FAAH) inhibitors that carbam

60 Fatty acid amide hydrolase (FAAH) is a degradative enzym

61 The metabolism of these lipids by fatty acid amide hydrolase (FAAH) is a key regulatory po

62 Fatty acid amide hydrolase (FAAH) is a mammalian amidase

63 Fatty acid amide hydrolase (FAAH) is a mammalian integra

64 Fatty acid amide hydrolase (FAAH) is a mammalian integra

65 Fatty acid amide hydrolase (FAAH) is a mammalian integra

66 Fatty acid amide hydrolase (FAAH) is a membrane-bound en

67 Fatty acid amide hydrolase (FAAH) is a membrane-bound en

68 Fatty acid amide hydrolase (FAAH) is a pharmaceutical ta

69 Fatty acid amide hydrolase (FAAH) is a serine hydrolase

70 Fatty acid amide hydrolase (FAAH) is a serine hydrolase

71 Fatty acid amide hydrolase (FAAH) is an integral membran

72 Fatty acid amide hydrolase (FAAH) is an integral membran

73 Fatty acid amide hydrolase (FAAH) is an integral membran

74 evels of endocannabinoids with inhibitors of fatty acid amide hydrolase (FAAH) is analgesic in models

75 Fatty acid amide hydrolase (FAAH) is one of the main enz

76 Once transported into the cytoplasm, fatty acid amide hydrolase (FAAH) is responsible for met

77 Fatty acid amide hydrolase (FAAH) knockout mice are pron

78 y-state time points (5 min), suggesting that fatty acid amide hydrolase (FAAH) may be responsible for

79 liana, and they can be metabolized by either fatty acid amide hydrolase (FAAH) or by lipoxygenase (LO

80 cal inhibition or genetic deletion of either fatty acid amide hydrolase (FAAH) or monoacylglycerol li

81 Fatty acid amide hydrolase (FAAH) plays a key role in re

82 ngle nucleotide polymorphisms CNR1 rs806378, fatty acid amide hydrolase (FAAH) rs324420, and MGLL rs4

83 Fatty acid amide hydrolase (FAAH) terminates the endocan

84 were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH) that additionally targ

85 A binding assay for human fatty acid amide hydrolase (FAAH) using the scintillatio

86 eral principle, the serine hydrolytic enzyme fatty acid amide hydrolase (FAAH) was found to degrade a

87 We show here that mice devoid of fatty acid amide hydrolase (FAAH) with elevated levels o

88 rease in side population (SP) cells, whereas fatty acid amide hydrolase (FAAH)(-/-) mice, which have

89 Fatty acid amide hydrolase (FAAH), a gene in the minimal

90 azole inhibitors (1 (OL-135) and 2) bound to fatty acid amide hydrolase (FAAH), a key enzymatic regul

91 ce of the eCB N-arachidonoylethanolamine via fatty acid amide hydrolase (FAAH), although it is unclea

92 Fatty acid amide hydrolase (FAAH), an amidase-signature

93 AEA is hydrolyzed by fatty acid amide hydrolase (FAAH), an enzyme localized o

94 l structure of the integral membrane protein fatty acid amide hydrolase (FAAH), an enzyme that degrad

95 endocytosis, and finally, to be degraded by fatty acid amide hydrolase (FAAH), an integral membrane

96 ting that following metabolism by the enzyme fatty acid amide hydrolase (FAAH), anandamide metabolite

97 endocannabinoid anandamide is hydrolysis by fatty acid amide hydrolase (FAAH), and inhibitors of the

98 erminated following hydrolysis by 2 enzymes: fatty acid amide hydrolase (FAAH), and the less-studied

99 L activity as well as their selectivity over fatty acid amide hydrolase (FAAH), another endocannabino

100 mes have been considered to serve this role: fatty acid amide hydrolase (FAAH), cyclooxygenase-2 (COX

101 The intracellular serine amidase, fatty acid amide hydrolase (FAAH), degrades a heterogene

102 nships of 2b (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed targeting

103 (SAR) of 2f (OL-135), a potent inhibitor of fatty acid amide hydrolase (FAAH), is detailed, targetin

104 ated by several metabolic enzymes, including fatty acid amide hydrolase (FAAH), monoacylglycerol lipa

105 inhibition of cyclooxygenase-2 (COX-2), not fatty acid amide hydrolase (FAAH), prolongs DSI, suggest

106 on, cloning, and expression of a rat enzyme, fatty acid amide hydrolase (FAAH), that degrades bioacti

107 incipal endocannabinoid-inactivating enzyme, fatty acid amide hydrolase (FAAH), that in homozygous fo

108 TFNO, an inhibitor of fatty acid amide hydrolase (FAAH), the enzyme responsibl

109 opment of exceptionally potent inhibitors of fatty acid amide hydrolase (FAAH), the enzyme responsibl

110 eripherally restricted inhibitor (URB937) of fatty acid amide hydrolase (FAAH), the enzyme responsibl

111 issense variant Pro129Thr of the gene coding fatty acid amide hydrolase (FAAH), the major degrading e

112 cluding the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH), triacylglycerol hydro

113 inhibition of endocannabinoid transport and fatty acid amide hydrolase (FAAH), two mechanisms of end

114 ignaling related to a common polymorphism in fatty acid amide hydrolase (FAAH), which alters endocann

115 HR1), evokes a rapid induction of the enzyme fatty acid amide hydrolase (FAAH), which causes a reduct

116 that promotes the cellular uptake of AEA and fatty acid amide hydrolase (FAAH), which hydrolyzes AEA

117 g activity is terminated by an enzyme called fatty acid amide hydrolase (FAAH), which hydrolyzes NAEs

118 bition of endocannabinoid hydrolyzing enzyme fatty acid amide hydrolase (FAAH), which leads to increa

119 hypoxic pulmonary vasoconstriction (HPV) via fatty acid amide hydrolase (FAAH)-dependent metabolites.

120 d 2-arachidonylglycerol) degradative enzyme, fatty acid amide hydrolase (FAAH)-IR, in the rat retina.

121 t negative growth-regulating properties, and fatty acid amide hydrolase (FAAH)-mediated hydrolysis is

122 were prepared and examined as inhibitors of fatty acid amide hydrolase (FAAH).

123 gulated by monoacylglycerol lipase (MGL) and fatty acid amide hydrolase (FAAH).

124 potent and systemically active inhibitor of fatty acid amide hydrolase (FAAH).

125 ovalent inhibitor of the EC-degrading enzyme fatty acid amide hydrolase (FAAH).

126 ediate AEA transport to its catabolic enzyme fatty acid amide hydrolase (FAAH).

127 strates for firefly luciferase by the enzyme fatty acid amide hydrolase (FAAH).

128 reduced activity of the AEA-degrading enzyme fatty acid amide hydrolase (FAAH).

129 es higher levels of the anandamide hydrolase fatty acid amide hydrolase (FAAH).

130 andamide is degraded by the catabolic enzyme fatty acid amide hydrolase (FAAH).

131 ing the anandamide-degrading membrane enzyme fatty acid amide hydrolase (FAAH).

132 s a potent in vitro and in vivo inhibitor of fatty acid amide hydrolase (FAAH).

133 nhibits cyclooxygenase-1 (COX-1), COX-2, and fatty acid amide hydrolase (FAAH).

134 bitors of monoacylglycerol lipase (MAGL) and fatty acid amide hydrolase (FAAH).

135 tors of the endocannabinoid-degrading enzyme fatty acid amide hydrolase (FAAH).

136 AEs) are primarily inactivated by the enzyme fatty acid amide hydrolase (FAAH).

137 unction with increased degradation of AEA by fatty acid amide hydrolase (FAAH).

138 Fatty acid amide hydrolase (FAAH, EC 3.5.1.99) is the ma

139 Mice lacking the enzyme fatty acid amide hydrolase [FAAH (-/-) mice] are severel

140 Nicotine exposure had no effect on fatty acid amide hydrolase activity in the VTA, suggesti

141 pharmacological profile in that it inhibits fatty acid amide hydrolase and alpha/beta-hydrolase doma

142 ing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase and did not display affinity

143 duced synergistic antiallodynic effects with fatty acid amide hydrolase and monoacylglycerol lipase i

144 bitors of endocannabinoid-regulating enzymes fatty acid amide hydrolase and monoacylglycerol lipase p

145 verall, the MAH data are similar to those of fatty acid amide hydrolase and support the suggestion th

146 udies revealed that NAPE-phospholipase D and fatty acid amide hydrolase are expressed in intestinal e

147 s of NAGly and its degradation by the enzyme fatty acid amide hydrolase can be observed in rat brain

148 rgan radiation exposure for the irreversible fatty acid amide hydrolase enzyme probe (11)C-CURB is wi

149 modulation of emotional states and point to fatty acid amide hydrolase inhibition as an innovative a

150 ferences following the administration of the fatty acid amide hydrolase inhibitor AM374.

151 ibiting their metabolizing enzymes URB597 (a fatty acid amide hydrolase inhibitor) and JZL184 (a mono

152 Independently of E2, a fatty acid amide hydrolase inhibitor, which blocks break

153 is of a retinoic acid receptor agonist and a fatty acid amide hydrolase inhibitor.

154 e phytocannabinoid cannabidiol and selective fatty acid amide hydrolase inhibitors has been proposed,

155 PalGly was up-regulated in fatty acid amide hydrolase knockout mice, suggesting a p

156 , N-acyltaurines, was recently discovered in fatty acid amide hydrolase knockout mice.

157 By combining fatty acid amide hydrolase or monoacyl glycerol lipase i

158 AEs are hydrolyzed intracellularly by either fatty acid amide hydrolase or N-acylethanolamine-hydroly

159 cerol lipase paralogs (DAGLalpha, DAGLbeta), fatty acid amide hydrolase paralogs (FAAH1, FAAH2), mono

160 sion of the Arabidopsis NAE degrading enzyme fatty acid amide hydrolase resulted in seedlings that we

161 oxylipin metabolites were identified in FAAH fatty acid amide hydrolase seedlings but not in wild-typ

162 ve MAGL inhibitor JZL184, in Mgll(-/-) mice, fatty acid amide hydrolase(-/-) mice, and in cannabinoid

163 Preventing their degradation (by inhibiting fatty acid amide hydrolase) enhanced the effects of OEA

164 f uptake (resulting in signal termination by fatty acid amide hydrolase) has been elusive.

165 EA synthesis, without concomitant changes in fatty acid amide hydrolase, an enzyme responsible for OE

166 These data contrast with blockade of fatty acid amide hydrolase, an enzyme that degrades the

167 availability of the X-ray structures of Pam, fatty acid amide hydrolase, and malonamidase E2 has led

168 dentified at the molecular level (designated fatty acid amide hydrolase, FAAH), and although an analo

169 chemically and described as an inhibitor of fatty acid amide hydrolase, had previously been found in

170 As with another member of this family, fatty acid amide hydrolase, MAH has the uncommon ability

171 also show that dCAD cells express functional fatty acid amide hydrolase, the enzyme primarily respons

172 ective and systemically active inhibitors of fatty acid amide hydrolase, the enzyme responsible for t

173 th as oleamide agonists and as inhibitors of fatty acid amide hydrolase, which is responsible for the

174 he intracellular anandamide-degrading enzyme fatty acid amide hydrolase-1 (FAAH-1), termed FAAH-like

175 pathways can be suggested: 1) inhibition of fatty acid amide hydrolase-induced increases in anandami

176 ty and expression of the OEAdegrading enzyme fatty acid amide hydrolase.

177 entiation of the anandamide catabolic enzyme fatty acid amide hydrolase.

178 1.80 fmol/mg protein) that is distinct from fatty acid amide hydrolase.

179 ivity of the anandamide-catabolizing enzyme, fatty acid amide hydrolase.

180 e than N-arachidonoylserotonin in inhibiting fatty acid amide hydrolase.

181 y of the endocannabinoid metabolizing enzyme fatty acid amide hydrolase.

182 Fatty-acid amide hydrolase (FAAH) is a membrane-bound en

183 in those cells containing an amidase called fatty-acid amide hydrolase (FAAH) is hydrolysis to arach

184 internalization, anandamide is hydrolyzed by fatty-acid amide hydrolase (FAAH), an intracellular memb

185 ill hereafter refer to oleamide hydrolase as fatty-acid amide hydrolase, in recognition of the plural

186 bitors of the anandamide-deactivating enzyme fatty-acid amide hydrolase, which selectively elevate an

187 transporter while being a poor substrate for fatty-acid amide hydrolase.

188 tion of arachidonic acid and ethanolamine by fatty-acid amide hydrolase.

189 The DEX effect was prevented by blocking fatty acid amide hydrolysis or by inhibiting anandamide

190 at oleamide hydrolase converts anandamide, a fatty-acid amide identified as the endogenous ligand for

191 ow the identification of fatty acids and the fatty acid amides in human meibomian gland secretions by

192 e, and human supports a general role for the fatty acid amides in mammalian biology.

193 anolamine-based compound and the presence of fatty acid amides in tissue prompts us to propose that p

194 Representative fatty acid amides include the N-acyl ethanolamines (NAEs

195 de hydrolase (FAAH) degrades neuromodulating fatty acid amides including anandamide (endogenous canna

196 nsible for the catabolism of neuromodulatory fatty acid amides, including anandamide and oleamide.

197 ng to the N-acyl ethanolamine (NAE) class of fatty acid amides, including the endocannabinoid anandam

198 ture enzyme that inactivates neuromodulatory fatty acid amides, including the endogenous cannabinoid

199 yme that catabolizes several neuromodulatory fatty acid amides, including the endogenous cannabinoid

200 he hydrolysis of a number of neuromodulatory fatty acid amides, including the endogenous cannabinoid

201 rolysis of a number of primary and secondary fatty acid amides, including the neuromodulatory compoun

202 Capsaicin, a vanillyl fatty acid amide (ingredient of hot pepper), released su

203 de hydrolase (FAAH), that degrades bioactive fatty acid amides like oleamide and anandamide to their

204 ne-bound enzyme that inactivates a family of fatty acid amide molecules which are implicated in physi

205 ified in a similar manner, as were the other fatty acid amides (myristamide, palmitamide, stearamide,

206 Fatty acid amides of polyamines may be rapidly cleared f

207 N4-Substituted fatty acid amide prodrugs of 10-16 carbon chain length d

208 vidence that PAM does have a role in primary fatty acid amide production in vivo.

209 ntly identified a second structural class of fatty acid amides regulated by FAAH in vivo: the N-acyl

210 The magnitude and duration of fatty acid amide signaling are controlled by enzymatic h

211 ntegrates into cell membranes and terminates fatty acid amide signaling in vivo.

212 elmidrol, an analog of the anti-inflammatory fatty acid amide signaling molecule palmitoylethanolamid

213 g genetic or pharmacological findings on the fatty acid amide signaling system across species.

214 sis, post-transcriptional gene silencing and fatty-acid amide signalling.

215 and membrane access channel responsible for fatty acid amide substrate and inhibitor acyl chain bind

216 ter as FAAH-1 and FAAH-2, hydrolyzed primary fatty acid amide substrates (e.g. oleamide) at equivalen

217 e-bound enzyme that degrades neuromodulatory fatty acid amides, such as oleamide and anandamide, and

218 s) in M. sexta represents direct evidence of fatty acid amide synthesis by caterpillar tissues.

219 N-Acylethanolamines (NAEs) are a group of fatty acid amides that play signaling roles in diverse p

220 ydrolase, in recognition of the plurality of fatty-acid amides that the enzyme can accept as substrat