ライフサイエンスコーパス: arachidonoyl

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

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

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

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

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

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

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

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

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

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

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

12 Oxidized arachidonoyl chains caused dose-dependent increases in p

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

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

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

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

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

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

19 Arachidonoyl-CoA synthetase and CoA-dependent transferas

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

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

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

23 ltransferase with remarkable specificity for arachidonoyl-CoA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

40 which include the mammalian endocannabinoid arachidonoyl ethanolamide.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

89 2-Arachidonoyl glycerol, an endocannabinoid, is one such m

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

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

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

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

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

95 The 2-arachidonoyl glycerol-induced phosphorylation of vasodil

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

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

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

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

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

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

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

103 N-arachidonoyl glycine is an endogenous arachidonoyl amide

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 1-alkenyl analogs of PAPC, and 1-palmitoyl-2-arachidonoyl phosphatidic acid or phosphoglycerol.

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

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

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

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

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

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

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

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

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

152 N-Arachidonoyl phosphatidylethanolamine-phospholipase D (N

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

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

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

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

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

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

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

160 841 for detection of 1-trideuterostearoyl-3-arachidonoyl-sn-2-glycerol employed as the internal stan

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

206 N-arachidonoyl taurine is therefore an interesting prototy

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

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