ライフサイエンスコーパス: arachidonoyl

1 rachidonoyl CoA and holding the main body of arachidonoyl.

2 exaenoyl (1.78%), eicosapentaenoyl (14.15%), arachidonoyl (0.92%) and gamma-linolenoyl (0.78%) sugges

3 '',6'',8'',9'',11'',12'',14'',15''-(3)H(N)]2-arachidonoyl-1,3-dibutyrylglycerol , a triacylglycerol t

4 pha signaling and employed in vitro binding, arachidonoyl-[1-(14)C]ethanolamide ([(14)C]AEA) uptake,

5 ed the TRPV1-specific synthetic cannabinoid, arachidonoyl-2 chloroethanolamine (ACEA), to study perip

6 lar infusions of either WIN55,212-2 (WIN) or arachidonoyl-2'-chloroethylamide (ACEA) while controllin

7 endocannabinoid, as well as the CB1 agonist arachidonoyl-2-chloroethylamide, prevent myotube formati

8 TM domain did not affect 2-AG or fluorogenic arachidonoyl, 7-hydroxy-6-methoxy-4-methylcoumarin ester

9 e peroxidation of PUFA-PLs, particularly sn2-arachidonoyl(AA)- and sn2-adrenoyl(AdA)-containing phosp

10 mmalian tissues are enriched in the stearoyl/arachidonoyl acyl chain species ("C38:4"), but its funct

11 responsible for enrichment of GPInsP n with arachidonoyl acyl chains.

12 N-arachidonoyl glycine is an endogenous arachidonoyl amide that activates the orphan G protein-c

13 e amino acids and one endocannabinoid (i.e., arachidonoyl amide), while compounds belonging to the cl

14 ted fatty acid (PUFA) acyl groups, including arachidonoyl and docosahexaenoyl.

15 ll three isoforms, but both the 1-stearoyl-2-arachidonoyl and the 1-stearoyl-2-oleoyl forms of PtdIns

16 zed by excessive accumulation of hydroperoxy-arachidonoyl (C20:4)- or adrenoyl (C22:4)- phosphatidyle

17 hat eicosanoid endocannabinoids harboring an arachidonoyl chain compete for a common membrane target

18 Oxidized arachidonoyl chains caused dose-dependent increases in p

19 zymes, and neutrophil microsomes incorporate arachidonoyl chains into phosphatidylinositol, phosphati

20 ine and lyso-PS to incorporate linoleoyl and arachidonoyl chains.

21 ic cholesterol metabolism-associated lipids [arachidonoyl cholesteryl ester, C8-dihydroceramide, N-st

22 ocket was found expanding the tunnel for the arachidonoyl CoA and holding the main body of arachidono

23 BC membranes from Ch-loaded RBCs, using [14C]arachidonoyl CoA as precursor, and found similar decreas

24 lar species (e.g., [3H]myristoyl CoA or [14C]arachidonoyl CoA), fatty acids (e.g., [14C]palmitic and

25 Thimerosal, an inhibitor of arachidonoyl- CoA:l-palmitoyl-sn-glycero-3-phosphocholin

26 Arachidonoyl-CoA synthetase and CoA-dependent transferas

27 (LCASs), including oleoyl-CoA synthetase and arachidonoyl-CoA synthetase, by 150-580% over control, b

28 ucture where the lysophosphatidylcholine and arachidonoyl-CoA were positioned in two tunnels connecte

29 idonic acid) and fatty acyl-CoA esters (e.g. arachidonoyl-CoA) has been reported.

30 > stearoyl-CoA >> oleoyl-CoA approximately = arachidonoyl-CoA) present either as monomers in solution

31 ltransferase with remarkable specificity for arachidonoyl-CoA.

32 (e.g. pamitoyl-, stearoyl-, linoleoyl-, and arachidonoyl-CoAs) yielded a single binding site with K(

33 ticipated significance of sn-1 hydrolysis of arachidonoyl-containing choline and ethanolamine glycero

34 saturation introduction at the corresponding arachidonoyl Delta(8,9)/Delta(11,12) and oleoyl Delta(9,

35 e termination of signals transmitted through arachidonoyl-diacylglycerol and/or the synthesis of phos

36 N-Arachidonoyl dopamine (NADA) is an endogenous lipid that

37 Metabolomics revealed that the level of N-arachidonoyl dopamine (NADA), an endocannabinoid, was de

38 thetic cannabinoid WIN55,212-2 and the eCB N-arachidonoyl dopamine (NADA), but neither anandamide nor

39 The endocannabinoids virodhamine and N-arachidonoyl dopamine are potent inhibitors of N-formyl-

40 -arachidonoyl-l-serine), anandamide, NADA (N-arachidonoyl dopamine), NATau (N-arachidonoyl taurine),

41 ass of lipids formed by the epoxidation of N-arachidonoyl-dopamine (NADA) and N-arachidonoyl-serotoni

42 ilability of biosynthetic precursors, that N-arachidonoyl-dopamine (NADA) is an endogenous "capsaicin

43 apsaicin (CAP) and the eCBs anandamide and N-arachidonoyl-dopamine elevated [Ca(2+) ]i in 30-40% of w

44 capsaicin or the endogenous TRPV1 agonist N-arachidonoyl-dopamine induces a prolonged elevation of p

45 steric site, including the endocannabinoids, arachidonoyl ethanolamide (anandamide) and 2-arachidonoy

46 cannabinoids are 2-arachidonoyl glycerol and arachidonoyl ethanolamide (anandamide).

47 The uptake of arachidonoyl ethanolamide (anandamide, AEA) in rat basop

48 ds (eCBs) 2-arachidonoyl glycerol (2-AG) and arachidonoyl ethanolamide by cyclooxygenase-2 (COX-2) pr

49 rally from the endocannabinoid anandamide (N-arachidonoyl ethanolamide) by a single oxygen atom even

50 ic levels of the endocannabinoid anandamide (arachidonoyl ethanolamide), CB(1) density, and basal rat

51 The endocannabinoid anandamide (arachidonoyl ethanolamide, AEA) is an uncharged neuromod

52 which include the mammalian endocannabinoid arachidonoyl ethanolamide.

53 The endocannabinoid arachidonoyl ethanolamine (anandamide) is a lipid transm

54 For example, N-arachidonoyl-ethanolamine and 2-arachidonoyl-glycerol ca

55 docannabinoids 2-arachidonoyl-glycerol and N-arachidonoyl-ethanolamine mediate an array of pro- and a

56 ide, and were completely prevented by methyl-arachidonoyl-fluorophosphate and palmostatin B, and part

57 substrate and the covalent inhibitor methyl arachidonoyl fluorophosphonate and located regions in th

58 3)H]HETE increased substantially when methyl arachidonoyl fluorophosphonate, but not bromoenol lacton

59 ges were seen in the presence of only methyl arachidonoyl fluorophosphonate.

60 V(max) was greater for the 1-stearoyl-2-arachidonoyl form compared with the 1-stearoyl-2-oleoyl

61 oleoyl L-alpha-phosphatidylcholine, and beta-arachidonoyl gamma-palmitoyl L-alpha-phosphatidylcholine

62 d the crystal structure of the 2-AG isomer 1-arachidonoyl glycerol (1-AG) in complex with wild type a

63 (LTD) was mediated by the endocannabinoid 2-arachidonoyl glycerol (2-AG) acting on a TRPV (transient

64 genation of endogenous cannabinoids (eCBs) 2-arachidonoyl glycerol (2-AG) and arachidonoyl ethanolami

65 The endocannabinoids (eCBs) anandamide and 2-arachidonoyl glycerol (2-AG) are inactivated by a two-st

66 ith elevated levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG) are protected from enteric

67 the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) are released by aversive tr

68 Bean (2017) show that the endocannabinoid 2-arachidonoyl glycerol (2-AG) can directly alter the prop

69 or agonist WIN55212-2 (10-30 ng/side), the 2-arachidonoyl glycerol (2-AG) hydrolysis inhibitor JZL184

70 drolase-induced increases in anandamide or 2-arachidonoyl glycerol (2-AG) levels, resulting in analge

71 exposure paradigms increased VTA dialysate 2-arachidonoyl glycerol (2-AG) levels.

72 n this study, we determined the effects of 2-arachidonoyl glycerol (2-AG) on hepatic stellate cells (

73 effects of endogenous anandamide (AEA) and 2-arachidonoyl glycerol (2-AG) on the permeability and inf

74 , and spinal cord levels of anandamide and 2-arachidonoyl glycerol (2-AG) were increased in MIA-treat

75 damide (arachidonoylethanolamide, AEA) and 2-arachidonoyl glycerol (2-AG), and of the AEA congener, p

76 in endogenous cannabinoids, anandamide and 2-arachidonoyl glycerol (2-AG), are produced on demand fro

77 ain endocannabinoids, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), are released in an activit

78 is itself occluded by the endocannabinoid 2-arachidonoyl glycerol (2-AG), consistent with 2-AG as a

79 or agonists, including the endocannabinoid 2-arachidonoyl glycerol (2-AG), for [35S]GTPgammaS binding

80 Endocannabinoid, particularly 2-arachidonoyl glycerol (2-AG), signaling has recently eme

81 eleases high levels of the endocannabinoid 2-arachidonoyl glycerol (2-AG), suggesting an alternative

82 he two eCB molecules, anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), with stress exposure reduc

83 nate endocannabinoid substrates, including 2-arachidonoyl glycerol (2-AG).

84 egulated hydrolysis of the endocannabinoid 2-arachidonoyl glycerol (2-AG).

85 after incubation with the endocannabinoid 2-arachidonoyl glycerol (2-AG).

86 ades since the discovery of anandamide and 2-arachidonoyl glycerol (2-AG).

87 e production of the endogenous cannabinoid 2-arachidonoyl glycerol (2-AG).

88 nts, i.e., free AA and the endocannabinoid 2-arachidonoyl glycerol (2-AG).

89 ), implicated in the production of the eCB 2-arachidonoyl glycerol (2-AG); monoacylglycerol lipase (M

90 espite similarities in chemical structure, 2-arachidonoyl glycerol and anandamide are synthesized and

91 n the CNS, early-life stress (1) decreased 2-arachidonoyl glycerol and arachidonic acid in the cerebe

92 e best-studied endogenous cannabinoids are 2-arachidonoyl glycerol and arachidonoyl ethanolamide (ana

93 cts of the endocannabinoids anandamide and 2-arachidonoyl glycerol are terminated by enzymatic hydrol

94 city of molecular rearrangements impairing 2-arachidonoyl glycerol availability and actions may diffe

95 In addition, we found that inhibition of 2-arachidonoyl glycerol biosynthesis blocked LTD induction

96 This study demonstrates that 2-arachidonoyl glycerol counteracts Ca(2+) mobilization an

97 situs nucleus in males only; (2) decreased 2-arachidonoyl glycerol in females only in cerebellar Crus

98 sis blocked LTD induction, suggesting that 2-arachidonoyl glycerol is the most likely retrograde eCB

99 These findings suggest that 2-arachidonoyl glycerol may contribute to the regulation o

100 have experimentally confirmed that altered 2-arachidonoyl glycerol signalling could contribute to syn

101 We hypothesized that errant retrograde 2-arachidonoyl glycerol signalling impairs synaptic neurot

102 sease progression slows the termination of 2-arachidonoyl glycerol signalling.

103 or endogenous cannabinoids (anandamide and 2-arachidonoyl glycerol) were identified only 20 to 25 yea

104 e fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol

105 e fatty acid amide hydrolase; or the 2-AG (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol

106 nctions as the main metabolizing enzyme of 2-arachidonoyl glycerol, an endocannabinoid signaling lipi

107 2-Arachidonoyl glycerol, an endocannabinoid, is one such m

108 ndothelin-1 with the putative vasorelaxant 2-arachidonoyl glycerol, an endogenous cannabimimetic deri

109 arachidonoyl ethanolamide (anandamide) and 2-arachidonoyl glycerol, and the plant-derived Delta(9)-te

110 ents, secoisolariciresinol diglucoside and 2-arachidonoyl glycerol, demonstrated protection by reduci

111 wo endocannabinoids, such as anandamide or 2-arachidonoyl glycerol, is insufficient to describe the b

112 pase alpha and beta isoforms, synthesizing 2-arachidonoyl glycerol, significantly increased in defini

113 potency, and efficacy of meth-anandamide, 2-arachidonoyl glycerol, virodhamine, Noladin ether, docos

114 We found that microglia, expressing two 2-arachidonoyl glycerol-degrading enzymes, serine hydrolas

115 The 2-arachidonoyl glycerol-induced phosphorylation of vasodil

116 f endogenous levels of AEA, and, possibly, 2-arachidonoyl glycerol-significantly ameliorated spastici

117 Endocannabinoid (eCB), 2-arachidonoyl-glycerol (2-AG), the most abundant eCB in t

118 The endocannabinoids 2-arachidonoyl-glycerol and N-arachidonoyl-ethanolamine me

119 r example, N-arachidonoyl-ethanolamine and 2-arachidonoyl-glycerol can be metabolized by cyclooxygena

120 nnabinoids, N-arachidonoylethanolamine and 2-arachidonoyl-glycerol, which derive from arachidonic aci

121 Subjecting purified 1-hexadecyl-2-arachidonoyl-glycerophosphocholine to UVB irradiation ge

122 The most widely studied member is N-arachidonoyl glycine (NAGly), which differs structurally

123 N-Oleoyl glycine and N-arachidonoyl glycine are structurally and functionally r

124 N-arachidonoyl glycine is an endogenous arachidonoyl amide

125 ch inhibit the Ca(v)3.3 current, as NAGly (N-arachidonoyl glycine), NASer (N-arachidonoyl-l-serine),

126 he production of N-oleoyl glycine and also N-arachidonoyl glycine.

127 yl-GPE (P-18:0/20:4), 1-(1-enyl-palmitoyl)-2-arachidonoyl-GPC (P-16:0/20:4), sulfate, and gamma-gluta

128 creatine, kynurenate, 1-(1-enyl-palmitoyl)-2-arachidonoyl-GPE (P-16:0/20:4), 1-(1-enyl-stearoyl)-2-ar

129 oyl-GPE (P-16:0/20:4), 1-(1-enyl-stearoyl)-2-arachidonoyl-GPE (P-18:0/20:4), 1-(1-enyl-palmitoyl)-2-a

130 ar leukocyte, it was found that the abundant arachidonoyl GPEtn plasmalogen molecular species were un

131 lysoPLA and PLA2 activities, but the rate of arachidonoyl group deacylation was increased by prior sn

132 of an sn-2-docosahexaenoyl group or an sn-2-arachidonoyl group increases the molecular areas of phos

133 The 95-kDa protein also deacylated arachidonoyl groups from 1-O-hexadecyl-2-arachidonoyl-PC

134 Moreover, the deacylation of arachidonoyl groups from diacylPC was greatly increased

135 oleoyl groups, and they were negligible for arachidonoyl groups.

136 were transferred into CL, but not oleoyl or arachidonoyl groups.

137 Although having no effect alone, N-arachidonoyl l-serine attenuated inhibition of human neu

138 is antagonized by the endogenous compound N-arachidonoyl l-serine.

139 as NAGly (N-arachidonoyl glycine), NASer (N-arachidonoyl-l-serine), anandamide, NADA (N-arachidonoyl

140 ourse of a 300-min oxidation, the ability of arachidonoyl lipids to accelerate prothrombinase peaked

141 ontaining lipid vesicles containing oxidized arachidonoyl lipids, and we examined their ability to ac

142 s spectrometric analysis demonstrated that 2-arachidonoyl LPC is a natural product in human myocardiu

143 The putative regiospecificity of the 2-arachidonoyl LPC product was authenticated by its diagno

144 ective pathway through iPLA2gamma-mediated 2-arachidonoyl LPC production to amplify and diversify the

145 iological relevance of iPLA2gamma-mediated 2-arachidonoyl LPC production utilizing naturally occurrin

146 Because 2-arachidonoyl LPC represents a key branch point intermedi

147 y identified the selective accumulation of 2-arachidonoyl LPC.

148 ospholipases to generate the corresponding 2-arachidonoyl-lysolipids.

149 tic acid and the selective accumulation of 2-arachidonoyl lysophosphatidylcholine (LPC), which was no

150 ults in the highly selective generation of 2-arachidonoyl lysophosphatidylcholine.

151 oselective and stereospecific oxidation of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-ar

152 Calcium ion stimulated the production of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) from 1-p

153 l-enantiomers) nonhydrolyzable analogs of 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC).

154 crylamide gel electrophoresis and deacylated arachidonoyl-lysophosphatidylcholine (ara-lysoPC) at rat

155 oyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-AA-LPE).

156 lipids, and the esterification of oxidized 2-arachidonoyl-lysophospholipids by acyl-CoA-dependent sn-

157 se- or lipoxygenase-catalyzed oxidation of 2-arachidonoyl-lysophospholipids produced from either phos

158 irect enzymatic oxidation of the resultant 2-arachidonoyl-lysophospholipids, and the esterification o

159 Hydroxy, hydroperoxy, and keto products of 2-arachidonoyl-lysoPI oxidation by 15-LO were identified b

160 o structurally distinct inhibitors of MGL [N-arachidonoyl maleimide and 4-nitrophenyl 4-(dibenzo[d][1

161 that the dipole moments of species having an arachidonoyl moiety or an oleoyl moiety are 83 mD (19%)

162 the formation of free arachidonic acid and O-arachidonoyl-N-acetylsphingosine was observed.

163 mino acid sequence) prefers sn-1-palmitoyl-2-arachidonoyl PC (PAPC).

164 ted arachidonoyl groups from 1-O-hexadecyl-2-arachidonoyl-PC (PLA2 activity) at a rate of 15 micromol

165 andamide (11 +/- 7 pmol/gm wet tissue) and N-arachidonoyl PE (22 +/- 16 pmol/gm), as assessed by gas

166 They also suggest that biosynthesis of N-arachidonoyl PE and formation of anandamide are tightly

167 cortical neurons prevents Ca2+-stimulated N-arachidonoyl PE biosynthesis.

168 n brain that catalyzes the biosynthesis of N-arachidonoyl PE by transferring an arachidonate group fr

169 The presence of N-arachidonoyl PE in adult brain tissue and the enzyme pat

170 e phosphatidylethanolamine (PE) derivative N-arachidonoyl PE.

171 e biosynthesis of the anandamide precursor N-arachidonoyl PE.

172 oleoylphosphatidylcholine:1-palmitoyl-2-[14C]arachidonoyl-phosphati dylethanolamine:sulfatide (70:0.2

173 a pathway for the selective translocation of arachidonoyl phosphatidic acid from the plasma membrane

174 1-alkenyl analogs of PAPC, and 1-palmitoyl-2-arachidonoyl phosphatidic acid or phosphoglycerol.

175 Oxidation of synthetic alkyl arachidonoyl phosphatidylcholine generated these C(4)-PA

176 oline (an oxidation product of 1-palmitoyl 2-arachidonoyl phosphatidylcholine) with serum albumin, sh

177 The proportion of sn-2-arachidonoyl-phosphatidylcholine (20:4-PC) inversely cor

178 inding to products of oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine (OxPAPC) and to the spe

179 idase activity with sn-2-linolenoyl- or sn-2-arachidonoyl-phosphatidylcholine hydroperoxides as subst

180 cPLA2beta has much lower activity on 2-arachidonoyl-phosphatidylcholine liposomes than either o

181 eicosanoid production derived from exogenous arachidonoyl-phosphatidylcholine, suggesting that PLB1 i

182 liposomes containing oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine.

183 ic cells through depleting immunosuppressive arachidonoyl phosphatidylcholines and oxidized derivativ

184 be generated from its membrane precursor, N-arachidonoyl phosphatidylethanolamine (NAPE) through cle

185 N-Arachidonoyl phosphatidylethanolamine-phospholipase D (N

186 A was produced from synthetic (1-stearoyl, 2-arachidonoyl)-phosphatidylethanolamine under saponificat

187 s to the accumulation of 15-hydroperoxy (Hp)-arachidonoyl-phosphatidylethanolamine (15-HpETE-PE), gen

188 ses the level of pro-ferroptotic hydroperoxy-arachidonoyl-phosphatidylethanolamine, reduces cardiomyo

189 (HAECs) generate proferroptotic hydroperoxy-arachidonoyl-phosphatidylethanolamines (HpETE-PEs) as pr

190 We identified 1-stearoyl-2-arachidonoyl-phosphatidylinositol (SAPI), which is the m

191 on of dengue virus infection by 1-stearoyl-2-arachidonoyl-phosphatidylinositol in vitro.

192 aroyl-2-docosahexaenoyl- and sn-1-stearoyl-2-arachidonoyl phosphoglycerides, but the structural signi

193 We also show that sn-1 arachidonoyl phospholipids are present in brain, where t

194 pholipase A(1)-mediated hydrolysis of diacyl arachidonoyl-phospholipids or through the cytochrome c-c

195 erential pathway of oxidative degradation of arachidonoyl plasmalogen GPE suggesting a unique role fo

196 ive hydrolysis of the vinyl ether linkage of arachidonoyl-plasmalogens.

197 g a biophysical basis for the requirement of arachidonoyl PLs in lipidating lipoprotein particles.

198 very low-density lipoprotein (VLDL) lacking arachidonoyl PLs.

199 15 knockout mice with 1-palmitoyl-2-oleoyl-3-arachidonoyl-rac-glycerol (C(57)H(100)O(6)), a top candi

200 ATau (N-arachidonoyl taurine), and NA-5HT (N-arachidonoyl serotonin), all displaced [(3)H]TTA-A1 bind

201 tion of N-arachidonoyl-dopamine (NADA) and N-arachidonoyl-serotonin (NA5HT) by epoxygenases.

202 841 for detection of 1-trideuterostearoyl-3-arachidonoyl-sn-2-glycerol employed as the internal stan

203 mined the effects of oxidized 1- palmitoyl-2-arachidonoyl-sn-3-glycero-phosphorylcholine (OxPAPC) on

204 toring m/z 838 for detection of 1-stearoyl-2-arachidonoyl-sn-3-glycerol and m/z 841 for detection of

205 imately 30 fmol) for endogenous 1-stearoyl-2-arachidonoyl-sn-3-glycerol per injection.

206 Conversion of 1-stearoyl-2-arachidonoyl-sn-3-glycerol to the pentafluorobenzoyl est

207 ith the precursor phospholipid 1-hexadecyl-2-arachidonoyl-sn-glycero-3-phosphocholine (HAPC) increase

208 re produced by autoxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC) and a

209 t fed rabbits, and autoxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (Ox-PAPC) that

210 Oxidized-l-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (ox-PAPC), a ma

211 Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (OxPAPC) and it

212 Thermal oxidation of the PUFA 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PAPC) created

213 (EC) response, the products of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PAPC) oxidatio

214 ds generated upon oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine (PAPC).

215 inflammatory lipids (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine [Ox-PAPC]) and

216 idized phospholipids (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine [OxPAPC]) promo

217 er, markedly elevated levels of 1-hydroxyl-2-arachidonoyl-sn-glycero-3-phosphocholine and 1-hydroxyl-

218 choline (2-AA-LPC) from 1-palmitoyl-2-[(14)C]arachidonoyl-sn-glycero-3-phosphocholine during incubati

219 incubation of iPLA2gamma with 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine resulted in the

220 specifically due to an increase in 1-acyl-2-arachidonoyl-sn-glycero-3-phosphocholine species, wherea

221 ontaining 6-10 mol % of 1-palmitoyl-2-[1-14C]arachidonoyl-sn-glycero-3-phosphocholine was employed.

222 nstrated that OxPAPC (oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine) significantly

223 gical agents, such as oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine, could also ind

224 luorogenic substrates, 1-O-(1-pyrenedecyl)-2-arachidonoyl-sn-glycero-3-phosphocholine, inserted in no

225 phospholipid from autoxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphocholine.

226 PE was from both 1-acyl- and 1-alk-1-enyl-2-arachidonoyl-sn-glycero-3-phosphoethanolamine species.

227 e interval [CI] = 0.48-0.87), and 1-oleoyl-2-arachidonoyl-sn-glycero-3-phosphoinositol (OR = 0.77; 95

228 Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (Ox-PAPC) an

229 Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (Ox-PAPC) an

230 rated previously that oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC) an

231 igated the effects of oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (ox-PAPC) on

232 phospholipids (oxPLs), such as 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (oxPAPC) and

233 RATIONALE: Oxidation of 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (OxPAPC) gen

234 ave demonstrated that oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (OxPAPC), a

235 Oxidized 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (OxPAPC), wh

236 abundant membrane phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC), whic

237 f the unsaturated phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-phosphocholine.

238 to uncover the role of the endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG) in controlling pain sens

239 The endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG) is produced through hydr

240 ndritic cells produce the endocannabinoid, 2-arachidonoyl-sn-glycerol (2-AG) upon antigen activation.

241 ds after AM251, increased endocannabinoid (2-arachidonoyl-sn-glycerol (2-AG)) levels in the taste org

242 nzyme that deactivates the endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG), exert anxiolytic-like e

243 n the mobilization of the endocannabinoid, 2-arachidonoyl-sn-glycerol (2-AG), in the amygdala.

244 the SI increases biosynthesis of the eCB, 2-arachidonoyl-sn-glycerol (2-AG), which drives hyperphagi

245 y degrading enzyme for the endocannabinoid 2-arachidonoyl-sn-glycerol (2-AG).

246 olytic deactivation of the endocannabinoid 2-arachidonoyl-sn-glycerol (2AG), is tightly controlled by

247 ilization of the 2-AG precursor 1-stearoyl,2-arachidonoyl-sn-glycerol and increased accumulation of t

248 etabotropic glutamate receptor-5-dependent 2-arachidonoyl-sn-glycerol formation is compromised.

249 a decrease in MAGL activity and increased 2-arachidonoyl-sn-glycerol levels in forebrain tissue.

250 Pharmacological enhancement of 2-arachidonoyl-sn-glycerol signalling normalizes this syna

251 , which is mediated by the endocannabinoid 2-arachidonoyl-sn-glycerol, is absent in fragile X mental

252 s metabotropic glutamate receptor-5 to the 2-arachidonoyl-sn-glycerol-producing enzyme, diacylglycero

253 i) inhibited LPS and oxidized 1-palmitoyl-2-arachidonoyl-sn-phosphatidylcholine (oxPAPC) dependent p

254 The enzyme showed selectivity for arachidonoyl-substituted lysoPC, since palmitoyl-lysoPC

255 N-arachidonoyl taurine is therefore an interesting prototy

256 ally, we find that the fatty acid analogue N-arachidonoyl taurine restores channel gating of many dif

257 de, NADA (N-arachidonoyl dopamine), NATau (N-arachidonoyl taurine), and NA-5HT (N-arachidonoyl seroto