ライフサイエンスコーパス: monoacylglycerol

1 ration of MGAT substrates (fatty acyl CoA or monoacylglycerol).

2 subsequent use by RAM2 to produce 16:0 beta-monoacylglycerol.

3 lglycerol-3-P followed by the deacylation of monoacylglycerol.

4 old greater for fatty acids as compared with monoacylglycerol.

5 t AtABHD11 hydrolyzed lyso(phospho)lipid and monoacylglycerol.

6 14 S complex, which is capable of acylating monoacylglycerol.

7 ited number of phase diagrams exists for the monoacylglycerols.

8 times faster from diacylglycerols than from monoacylglycerols.

9 y the esterification of free fatty acids and monoacylglycerols.

10 s not accomplished in the same yields as for monoacylglycerols.

11 nnabinoid 2-arachidonoylglycerol and related monoacylglycerols.

12 he MAGL substrate profile beyond the classic monoacylglycerols.

13 alyzing the release of free fatty acids from monoacylglycerols.

14 synthesis to increase the production of beta-monoacylglycerols.

15 te the effects of lecithin (0-0.4 g/100 ml), monoacylglycerol (0-0.4 g/100 ml), locust bean gum (LBG;

16 al (Li+) adducts and halide (Cl-) adducts of monoacylglycerol, 1,2-diacylglycerol, and 1,3-diacylglyc

17 Also studied were lithium-bound dimers of monoacylglycerols, 1,2-diacylglycerols, and 1,3-diacylgl

18 d with other unsaturated and polyunsaturated monoacylglycerols, 1,2-diacylglycerols, and fatty acids.

19 ss a phosphatase domain that results in sn-2 monoacylglycerol (2-MAG) rather than LPA as the major pr

20 tics of activation and inhibition of hepatic monoacylglycerol acyltransferase (MGAT) (EC 2.3.1.22) by

21 The activity of hepatic monoacylglycerol acyltransferase (MGAT) (EC 2.3.1.22), a

22 enterocytes, a process catalyzed by acyl-CoA:monoacylglycerol acyltransferase (MGAT) 2.

23 Monoacylglycerol acyltransferase (MGAT) catalyzes the sy

24 Acyl CoA:monoacylglycerol acyltransferase (MGAT) catalyzes the sy

25 Acyl coenzyme A:monoacylglycerol acyltransferase (MGAT) catalyzes the sy

26 Acyl-CoA:monoacylglycerol acyltransferase (MGAT) catalyzes the sy

27 Monoacylglycerol acyltransferase (MGAT) enzymes convert

28 Acyl-CoA:monoacylglycerol acyltransferase (MGAT) plays an importa

29 n assay, we found that DGAT2 interacted with monoacylglycerol acyltransferase (MGAT)-2, an enzyme tha

30 her acyltransferases, including the acyl-CoA:monoacylglycerol acyltransferase 1 and 2 enzymes and the

31 Monoacylglycerol acyltransferase 3 (MGAT3) is an integra

32 es cerevisiae have been shown to have both a monoacylglycerol acyltransferase and a phospholipase A(2

33 Phosphorylated OLE3 exhibited reduced monoacylglycerol acyltransferase and increased phospholi

34 , Oleosin3 (OLE3), was shown to exhibit both monoacylglycerol acyltransferase and phospholipase A(2)

35 ver, targeted deletion of the primary murine monoacylglycerol acyltransferase does not quantitatively

36 Acyl-CoA:monoacylglycerol acyltransferase-2 (MGAT2) catalyzes the

37 e intestinal lipid synthesis enzyme acyl CoA:monoacylglycerol acyltransferase-2 (MGAT2) has a crucial

38 Acyl-CoA:monoacylglycerol acyltransferases (MGATs) and diacylglyc

39 racterization of several intestinal acyl CoA:monoacylglycerol acyltransferases; these may provide new

40 ficity toward fatty acyl-CoA derivatives and monoacylglycerols, among which the highest activities we

41 te of diffusional transfer of fatty acid and monoacylglycerol analogues was approximately 30-fold gre

42 how that SMc01003 converts diacylglycerol to monoacylglycerol and a fatty acid, and that monoacylglyc

43 of G protein-coupled receptor (GPR) 119 by 2-monoacylglycerol and by the activation of fatty acid rec

44 -mannnosyl1-3 (6'-O-acyl alpha-mannosyl)-1-1 monoacylglycerol and cholesteryl 6'-O-acyl alpha-mannosi

45 ylglycerol kinase (AGK), that phosphorylates monoacylglycerol and diacylglycerol to form LPA and PA,

46 tered separately, both digestion products, 2-monoacylglycerol and fatty acids, were sensed by the mic

47 differing behavioural effects produced by 2-monoacylglycerol and fatty acids.

48 yzes the synthesis of diacylglycerol using 2-monoacylglycerol and fatty acyl coenzyme A.

49 is, GPAT5 produced very-long-chain saturated monoacylglycerols and free fatty acids as novel componen

50 trometry as diacylglycerol, free fatty acid, monoacylglycerol, and lysophosphatidylcholine.

51 ent signalling pathways by fatty acids and 2-monoacylglycerol, and suggest that the structural proper

52 yze the acylation of rac-1-, sn-2-, and sn-3-monoacylglycerols, and the enzyme prefers monoacylglycer

53 Absorbed fatty acids and monoacylglycerols are required to be bound to intracellu

54 These results provide strong support for monoacylglycerol as a physiological ligand for LFABP and

55 Radiolabeling identified sn-2 monoacylglycerol as an initial glycerolipid intermediate

56 l small intestine, releasing fatty acids and monoacylglycerol as the ultimate products.

57 o wild-type enzymes that hydrolyzed 1- and 2-monoacylglycerols at similar rates, mutation of Cys242 t

58 of phase behavior prediction for a specific monoacylglycerol based on an analysis of the existing ph

59 o investigate the transfer of fatty acid and monoacylglycerol between micelles.

60 r194 did not bias the hydrolysis of 1- and 2-monoacylglycerols but significantly compromised overall

61 monoacylglycerol and a fatty acid, and that monoacylglycerol can be further degraded by SMc01003 to

62 ing McArdle rat hepatoma RH7777 cells with 2-monoacylglycerol caused DGAT2 to translocate to lipid dr

63 Increasing monoacylglycerol concentration led to an increase in par

64 -3-monoacylglycerols, and the enzyme prefers monoacylglycerols containing unsaturated fatty acyls as

65 MGAT2 appeared to acylate monoacylglycerols containing unsaturated fatty acyls in

66 DGAT1, and indicated that DGAT2 can utilize monoacylglycerol-derived diacylglycerol.

67 h coincidental increases in free fatty acid, monoacylglycerol, diacylglycerol and phospholipid conten

68 r, the candidate lipid signaling molecules 1-monoacylglycerol, diacylglycerol, and malonyl-CoA; the p

69 chondrial membrane potential, ADP, Ca(2+), 1-monoacylglycerol, diacylglycerol, malonyl-CoA, and HMG-C

70 Fatty acids and monoacylglycerols entering the enterocyte via the basola

71 sed mainly of diacylglycerol ethers (10.6%), monoacylglycerol ethers (32.9%) and fatty acid ethyl est

72 h, giving a final product mainly composed of monoacylglycerol ethers (36.6%) and fatty acid ethyl est

73 S multiprotein complex capable of acylating monoacylglycerol from the microsomal membranes of develo

74 nd corticosterone together with increases in monoacylglycerol, glycerol, and medium- and long-chain f

75 olase domain-containing 6 (ABHD6) can act as monoacylglycerol hydrolase and is believed to play a rol

76 = 4.1 muM; IC(50) (30) = 2.4 muM), rat brain monoacylglycerol hydrolysis (IC(50) (8) = 1.8 muM; IC(50

77 ining the rate and the isomer preferences of monoacylglycerol hydrolysis.

78 ves their hydrolysis to free fatty acids and monoacylglycerols in the intestinal lumen, the uptake of

79 tion with the production of various 1- and 2-monoacylglycerols, including 2-AG, whereas stimulation o

80 -) mice, whereas LFABP(-/-) mice had reduced monoacylglycerol incorporation in TG relative to PL, as

81 .2, 0.4, 0.045, and 0.015 g/100 ml lecithin, monoacylglycerol, LBG and carrageenan, respectively.

82 uptake, lipid droplet size, or tri-, di-, or monoacylglycerol levels when compared with a control adi

83 work we report a new series of inhibitors of monoacylglycerol lipase (MAGL) and fatty acid amide hydr

84 Monoacylglycerol lipase (MAGL) and fatty acid amide hydr

85 a et al. now demonstrate that an increase in monoacylglycerol lipase (MAGL) drives tumorigenesis thro

86 at a distinct pathway exists in brain, where monoacylglycerol lipase (MAGL) hydrolyzes the endocannab

87 fects of both systemic pretreatment with the monoacylglycerol lipase (MAGL) inhibitor MJN110 (which s

88 Monoacylglycerol lipase (MAGL) inhibitors are considered

89 recent years in developing selective, potent monoacylglycerol lipase (MAGL) inhibitors.

90 Here, we show that the enzyme monoacylglycerol lipase (MAGL) is highly expressed in ag

91 Monoacylglycerol lipase (MAGL) is responsible for signal

92 Monoacylglycerol lipase (MAGL) links these pathways, hyd

93 on of the endocannabinoid catabolic enzymes, monoacylglycerol lipase (MAGL) or fatty acid amide hydro

94 Monoacylglycerol lipase (MAGL) represents a primary degr

95 JZL184, a potent and selective inhibitor for monoacylglycerol lipase (MAGL) that hydrolyzes 2-AG, ind

96 enzymatic hydrolysis, mainly carried out by monoacylglycerol lipase (MAGL), along with a small contr

97 l lipase (DAGL) or the 2-AG-degrading enzyme monoacylglycerol lipase (MAGL), and assessing the therap

98 either fatty acid amide hydrolase (FAAH) or monoacylglycerol lipase (MAGL), enzymes that regulate th

99 including fatty acid amide hydrolase (FAAH), monoacylglycerol lipase (MAGL), N-acylethanolamine acid

100 the antidepressant actions of inhibitors of monoacylglycerol lipase (MAGL), the major degradative en

101 We showed previously that inhibition of monoacylglycerol lipase (MAGL), the primary enzyme that

102 sm was produced by sustained inactivation of monoacylglycerol lipase (MAGL), the principal degradativ

103 the authors show that genetic disruption of monoacylglycerol lipase (MAGL), the principal degradativ

104 2-AG is degraded primarily by monoacylglycerol lipase (MAGL), which is expressed in ne

105 L), which biosynthesizes 2-AG, inhibition of monoacylglycerol lipase (MAGL), which metabolizes 2-AG,

106 ylglycerol (2-AG) is hydrolysed primarily by monoacylglycerol lipase (MAGL).

107 ylglycerol (2-AG) is hydrolyzed primarily by monoacylglycerol lipase (MAGL).

108 hydrolyzed primarily by the serine hydrolase monoacylglycerol lipase (MAGL).

109 rachidonoylglycerol (2-AG) is inactivated by monoacylglycerol lipase (MAGL).

110 n of the eCB 2-arachidonoyl glycerol (2-AG); monoacylglycerol lipase (MGL) and alpha/beta-hydrolase d

111 sted whether PG-G levels may be regulated by monoacylglycerol lipase (MGL) and fatty acid amide hydro

112 The serine hydrolase monoacylglycerol lipase (MGL) functions as the main meta

113 ydrolysis and demonstrated expression of the monoacylglycerol lipase (MGL) gene in human intestinal C

114 y of compound 4a, a potent beta-lactam-based monoacylglycerol lipase (MGL) inhibitor characterized by

115 have shown previously that overexpression of monoacylglycerol lipase (MGL), a cytosolic serine hydrol

116 The function of monoacylglycerol lipase (MGL), a key actor in the hydrol

117 hydrolase (FAAH), cyclooxygenase-2 (COX-2), monoacylglycerol lipase (MGL), and alpha/beta-hydrolase

118 ju3p, the functional orthologue of mammalian monoacylglycerol lipase (MGL), contributes >90% of cellu

119 In doing so, NGF limits the sorting of monoacylglycerol lipase (MGL), rate limiting 2-AG bioava

120 Furthermore, we show that astrocytes express monoacylglycerol lipase (MGL), the main hydrolyzing enzy

121 temic or local pharmacological inhibition of monoacylglycerol lipase (MGL)-a lipid hydrolase that deg

122 atty acid amide hydrolase (FAAH) and 2-AG by monoacylglycerol lipase (MGL).

123 Here, monoacylglycerol lipase accumulates in CB(1) cannabinoid

124 These studies also identify monoacylglycerol lipase as a previously unrecognized the

125 ls containing hyperphosphorylated tau retain monoacylglycerol lipase expression, although at levels s

126 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase in hippocampal neurons: serine h

127 increases in 2-AG levels obtained following monoacylglycerol lipase inhibition.

128 th GAT211, but it was not preserved with the monoacylglycerol lipase inhibitor JZL184.

129 Indeed, the specific monoacylglycerol lipase inhibitor URB602 prevented Trans

130 erone, the CB1R agonist WIN 55,212-2, or the monoacylglycerol lipase inhibitor URB602.

131 cid amide hydrolase inhibitor) and JZL184 (a monoacylglycerol lipase inhibitor).

132 effects with fatty acid amide hydrolase and monoacylglycerol lipase inhibitors in paclitaxel-treated

133 yzing enzyme ABHD6 (intracellular WWL70) and monoacylglycerol lipase MGL (JZL184) or by blocking GABA

134 r, inhibition of the eCB deactivating enzyme monoacylglycerol lipase normalized eCB-LTD in mBACtgDyrk

135 ating enzymes fatty acid amide hydrolase and monoacylglycerol lipase produce reliable antinociceptive

136 Subcellular fractionation revealed impaired monoacylglycerol lipase recruitment to biological membra

137 tion enzymes, fatty acid amid hydrolase, and monoacylglycerol lipase than males, and lower amounts of

138 This inverse sensitivity of DG lipase and monoacylglycerol lipase to calcium constitutes an origin

139 ng phospholipase A, lysophospholipase A, and monoacylglycerol lipase, although they are potential can

140 6, abhydrolase domain-containing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase

141 alpha/beta-hydrolase domain-containing 6 and monoacylglycerol lipase, begin to surround senile plaque

142 achidonoylglycerol (2-AG) degradation enzyme monoacylglycerol lipase, indicating that it is mediated

143 lipases, including hormone-sensitive lipase, monoacylglycerol lipase, lipoprotein lipase, and patatin

144 Enzymes that hydrolyze 2-AG, such as monoacylglycerol lipase, regulate the accumulation and e

145 d inhibitor of the 2-AG-deactivating enzyme, monoacylglycerol lipase, selectively increases 2-AG conc

146 se activity while inhibiting the activity of monoacylglycerol lipase, the enzyme that degrades 2-AG.

147 a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2

148 a potent reversible inhibitor of the enzyme monoacylglycerol lipase, which accounts for 85% of the 2

149 se and alpha/beta-hydrolase domain 6 but not monoacylglycerol lipase.

150 ted activity should be viewed as an esterase-monoacylglycerol lipase.

151 reased expression of its degradative enzyme, monoacylglycerol lipase.

152 Monoacylglycerol lipases (MGLs) play an important role i

153 and possibly the enzymes diacylglycerol and monoacylglycerol lipases to yield free AA.

154 enzyme that catalyzes the acylation of both monoacylglycerol (MAG) and diacylglycerol (DAG) to gener

155 , and enzyme assays revealed the presence of monoacylglycerol (MAG) and lysophosphatidylcholine (LPC)

156 Pretreatment with the monoacylglycerol (MAG) lipase inhibitor JZL-184 also red

157 mined the effect of diacylglycerol (DAG) and monoacylglycerol (MAG) on the oxidative stability of str

158 sses robust enzymatic activity for acylating monoacylglycerol (MAG).

159 such as sodium stearoyl lactylate (SSL) and monoacylglycerols (MAG) and Bacillus stearothermophilus

160 ork was to produce diacylglycerols (DAG) and monoacylglycerols (MAG) with a high content of polyunsat

161 Production of monoacylglycerols (MAGs) rich in omega-3 polyunsaturated

162 Nevertheless, the binding and transport of monoacylglycerol (MG) by LFABP are uncertain, with confl

163 Intestinal monoacylglycerol (MG) metabolism is well known to involv

164 Free fatty acids (FFA) and sn-2-monoacylglycerol (MG), the two major hydrolysis products

165 catalyzes the self-transesterification of 2-monoacylglycerol of 9(10),16-dihydroxyhexadecanoic acid,

166 ycerol digestion products, fatty acids and 2-monoacylglycerol, on behavioural, hormonal and dopaminer

167 We propose a model in which beta-monoacylglycerols, or a derivative thereof, are exported

168 that the synthesis of glycerolipids via the monoacylglycerol pathway may be highly regulated via a v

169 reesterified into TG, primarily through the monoacylglycerol pathway.

170 dextrin in reducing both cholesterol and bis(monoacylglycerol) phosphate accumulation in NPC mutant f

171 ecursor for synthesis of cardiolipin and bis(monoacylglycerol) phosphate.

172 triacylglycerols and diacylglycerols but not monoacylglycerols, phospholipids, galactolipids, or chol

173 contour plots illustrated that lecithin and monoacylglycerol played a dominant role in controlling t

174 rase and phosphatase activity resulting in 2-monoacylglycerol products.

175 he molecular speciation of free fatty acids, monoacylglycerol species, unmodified and oxidized phosph

176 id, lysophosphatidylcholine, diacylglycerol, monoacylglycerol, spermidine, amyloid-beta, amylin, and

177 evealed that the three enzymes have distinct monoacylglycerol substrate and isomer preferences.

178 ose hydrolysis rate rivaled that of the best monoacylglycerol substrates.

179 metabolism of not only fatty acids but also monoacylglycerol, the two major products of dietary tria

180 cerol acyltransferase (MGAT) enzymes convert monoacylglycerol to diacylglycerol, which is the penulti

181 solic serine hydrolase that cleaves 1- and 2-monoacylglycerols to fatty acid and glycerol, reduces st

182 Nevertheless, fatty acid and monoacylglycerol transfer from unilamellar vesicles coul

183 Acyl-CoA:monoacylglycerol transferase (MGAT) plays a predominant

184 [3H]delta4Ach-containing diacylglycerol and monoacylglycerol were apparent along the time course of

185 acetyl-CoA, H2O2, reduced glutathione, and 2-monoacylglycerol were not glucose-responsive.

186 y 5-lipooxygenase-derived metabolites, while monoacylglycerols were negatively correlated with body m

187 d in insect Sf9 cells selectively acylates 2-monoacylglycerol with higher efficiency than other stere

188 turated triacylglycerol, diacylglycerol, and monoacylglycerol with palmitate and myristate acyl chain

189 t amounts of both alpha- and beta-isomers of monoacylglycerols with C22 and C24 saturated acyl groups

190 cohols such as sterols, diacylglycerols, and monoacylglycerols with fatty acids represents the format

191 ajor glycerolipids, TAG, diacylglycerol, and monoacylglycerol, with a strong preference for oleic aci