ライフサイエンスコーパス: monoacylglycerol

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

2 14 S complex, which is capable of acylating monoacylglycerol.

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

4 old greater for fatty acids as compared with monoacylglycerol.

5 of fatty acid as well as triacylglycerol and monoacylglycerol.

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

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

8 alyzing the release of free fatty acids from monoacylglycerols.

9 ted to the high degree of micellarization of monoacylglycerols.

10 ited number of phase diagrams exists for the monoacylglycerols.

11 regulates 2-AG levels may also affect other monoacylglycerols.

12 n the brain and the hydrolysis of peripheral monoacylglycerols.

13 ipid classes and even more than 100-fold for monoacylglycerols.

14 synthesis to increase the production of beta-monoacylglycerols.

15 times faster from diacylglycerols than from monoacylglycerols.

16 y the esterification of free fatty acids and monoacylglycerols.

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

18 nnabinoid 2-arachidonoylglycerol and related monoacylglycerols.

19 he MAGL substrate profile beyond the classic monoacylglycerols.

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

21 decreased the limit of detection 9-fold for monoacylglycerols (0.9-1.0 nmol/mL), 6.5-fold for sphing

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

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

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

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

26 hly activated glycolysis, fatty acid (FA), 2-monoacylglycerol (2-MAG), and membrane lipid biosynthesi

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

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

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

30 Monoacylglycerol acyltransferase (MGAT) catalyzes the sy

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

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

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

34 Monoacylglycerol acyltransferase (MGAT) enzymes convert

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

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

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

38 ytes confirmed several factors including the monoacylglycerol acyltransferase 2 (MOGAT2) gene as a bo

39 Monoacylglycerol acyltransferase 3 (MGAT3) is an integra

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

41 Phosphorylated OLE3 exhibited reduced monoacylglycerol acyltransferase and increased phospholi

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

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

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

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

46 Unlike overexpression of Dgat1a and Dgat1b, monoacylglycerol acyltransferase-3 (Mogat3b) overexpress

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

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

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

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

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

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

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

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

55 s in small intestinal enterocytes utilizes 2-monoacylglycerol and does not require the PAP reaction,

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

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

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

59 rsion of lysophosphatidylinositol (LPI) into monoacylglycerol and inositol-1-phosphate.

60 tion spectra of tetramethylsilyl-derivatized monoacylglycerols and diacylglycerols are dominated by m

61 In brief, several monoacylglycerols and FA16:0 and FA18:0 in diacylglycero

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

63 N-acylamino acids, N-acylneurotransmitters, monoacylglycerols and primary fatty acid amides using 7

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

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

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

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

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

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

70 nor transacylation activity upon offering of monoacylglycerol as substrate.

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

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

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

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

75 y of GPAT4, GPAT6, and GPAT8, which leads to monoacylglycerol biosynthesis, contributes to suberin fo

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

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

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

79 es a specific lysoform lipoprotein (N-acyl S-monoacylglycerol) chemotype by an unknown mechanism that

80 Increasing monoacylglycerol concentration led to an increase in par

81 -3-monoacylglycerols, and the enzyme prefers monoacylglycerols containing unsaturated fatty acyls as

82 MGAT2 appeared to acylate monoacylglycerols containing unsaturated fatty acyls in

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

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

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

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

87 enerally, we detected more lipid species for monoacylglycerols, diacylglycerols, and sphingoid bases

88 e gas chromatography separations for mapping monoacylglycerols, diacylglycerols, and triacylglycerols

89 c acid is developed for the determination of monoacylglycerols, diacylglycerols, free sterols, and to

90 is identified enrichment of diacylglycerols, monoacylglycerols, diacylglycerophosphoethanolamines, mo

91 the disintegration of diacylglycerides into monoacylglycerols, disordering of the crystalline region

92 onversely, lipolysis breakdown products like monoacylglycerols (e.g., MG(16:0), MG(18:0)), diacylglyc

93 Fatty acids and monoacylglycerols entering the enterocyte via the basola

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

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

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

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

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

99 = 4.1 muM; IC(50) (30) = 2.4 muM), rat brain monoacylglycerol hydrolysis (IC(50) (8) = 1.8 muM; IC(50

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

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

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

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

104 .2, 0.4, 0.045, and 0.015 g/100 ml lecithin, monoacylglycerol, LBG and carrageenan, respectively.

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

106 increase of diacylglycerols and, especially, monoacylglycerols levels in fermented walnuts confirmed

107 Inhibition of human Monoacylglycerol Lipase (hMGL) offers a novel approach f

108 Monoacylglycerol lipase (MAGL) activity was evaluated in

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

110 Monoacylglycerol lipase (MAGL) and fatty acid amide hydr

111 ppression of inhibition (DSI) was limited by monoacylglycerol lipase (MAGL) but not by fatty acid ami

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

113 ntly associated with regional differences in monoacylglycerol lipase (MAGL) expression in postmortem

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

115 2-arachidonoylglycerol with a low dose of a monoacylglycerol lipase (MAGL) inhibitor facilitates mot

116 Inhibiting 2-AG degradation with the monoacylglycerol lipase (MAGL) inhibitor JZL184 during i

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

118 Monoacylglycerol lipase (MAGL) inhibitors are considered

119 New potent, selective monoacylglycerol lipase (MAGL) inhibitors based on the a

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

121 Monoacylglycerol lipase (MAGL) is a hydrolase involved i

122 Monoacylglycerol lipase (MAGL) is a key enzyme involved

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

124 Monoacylglycerol lipase (MAGL) is one of the key enzymes

125 Monoacylglycerol lipase (MAGL) is responsible for signal

126 Monoacylglycerol lipase (MAGL) is the enzyme degrading t

127 Monoacylglycerol lipase (MAGL) is the enzyme responsible

128 Monoacylglycerol lipase (MAGL) is the key enzyme for the

129 Monoacylglycerol lipase (MAGL) is the pivotal catabolic

130 Monoacylglycerol lipase (MAGL) links these pathways, hyd

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

132 Monoacylglycerol lipase (MAGL) regulates endocannabinoid

133 Monoacylglycerol lipase (MAGL) represents a primary degr

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

135 recent efforts have focused on inhibition of monoacylglycerol lipase (MAGL) to enhance signaling of t

136 n addition, a series of tetrazine probes for monoacylglycerol lipase (MAGL) were synthesized and the

137 Inhibition of monoacylglycerol lipase (MAGL) with JZL184 increases the

138 Monoacylglycerol lipase (MAGL), a serine hydrolase exten

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

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

141 ological inhibition of its catabolic enzyme, monoacylglycerol lipase (MAGL), either systemically or i

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

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

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

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

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

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

148 novel transcriptional target MGLL, encoding monoacylglycerol lipase (MAGL), to regulate the self-ren

149 2-AG is degraded primarily by monoacylglycerol lipase (MAGL), which is expressed in ne

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

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

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

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

154 n 5 (FABP5), fatty acid synthase (FASN), and monoacylglycerol lipase (MAGL).

155 18)F]YH134 as a novel PET tracer for imaging monoacylglycerol lipase (MAGL).

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

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

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

159 iators of the inflammatory response, such as monoacylglycerol lipase (MGL) and fatty acid amide hydro

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

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

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

163 Monoacylglycerol lipase (MGL) is the last enzymatic step

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

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

166 e in high-fat diet (HFD)-induced obesity for monoacylglycerol lipase (MGL), an enzyme that is also kn

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

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

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

170 Inhibitors of monoacylglycerol lipase (MGL), the enzyme that deactivat

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

172 Z) derivatives that are potent inhibitors of monoacylglycerol lipase (MGL), the primary degrading enz

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

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

175 d eicosanoid lipids by DAG lipase (DAGL) and monoacylglycerol lipase (MGLL) enzymes in innate immune

176 h expression of the serine hydrolase enzymes monoacylglycerol lipase (MGLL) or carboxylesterase 1 (CE

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

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

179 In contrast, pharmacologic inhibition of monoacylglycerol lipase attenuates GBM proliferation.

180 Monoacylglycerol lipase deficiency affects diet-induced

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

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

183 protective effects produced by inhibition of monoacylglycerol lipase in traumatic brain injury remain

184 nalling in astrocytes is responsible for the monoacylglycerol lipase inactivation-produced alleviatio

185 The monoacylglycerol lipase inactivation-produced neuroprote

186 This study shows an additive mechanism (monoacylglycerol lipase inhibition) by which BCP might i

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

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

189 Indeed, the specific monoacylglycerol lipase inhibitor URB602 prevented Trans

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

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

192 augmentation via administration of JZL184, a monoacylglycerol lipase inhibitor, blocked SI deficits a

193 enzyme that reacts potently with a covalent monoacylglycerol lipase inhibitor.

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

195 l RNA-sequencing data reveal that astrocytic monoacylglycerol lipase knockout mice display greater re

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

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

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

199 Subcellular fractionation revealed impaired monoacylglycerol lipase recruitment to biological membra

200 Here we first show that genetic deletion of monoacylglycerol lipase reduces neuropathology and avert

201 oscopy to selectively activate intracellular monoacylglycerol lipase tagged with DHTz-labeled small m

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

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

204 t neurons are rescued by inhibition of MGLL (monoacylglycerol lipase), the enzyme responsible for 2-A

205 es showed that pharmacological inhibition of monoacylglycerol lipase, a key enzyme degrading the endo

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

207 6, abhydrolase domain-containing protein 12, monoacylglycerol lipase, and fatty acid amide hydrolase

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

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

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

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

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

213 c (10 days) JZL184, a selective inhibitor of monoacylglycerol lipase, specifically normalized the soc

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

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

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

217 reased expression of its degradative enzyme, monoacylglycerol lipase.

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

219 increased degradation of endocannabinoids by monoacylglycerol lipase.

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

221 e (ATGL) and not hormone-sensitive lipase or monoacylglycerol lipase.

222 G (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol lipase.

223 G (2-arachidonoyl glycerol)-degrading enzyme monoacylglycerol lipase.

224 Monoacylglycerol lipases (MGLs) play an important role i

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

226 acid alkyl esters and their combination with monoacylglycerol (MAG) and 1,2-dioleoyl-sn-glycero-3-pho

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

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

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

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

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

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

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

234 Monoacylglycerols (MAGs) are active mediators involved i

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

236 atty acid (FA) 20:4 containing DAGs, FA 20:4 monoacylglycerols (MAGs), and FA 20:4 with PGE(2) and di

237 st and selective separation method of intact monoacylglycerol (MG) and diacylglycerol (DG) isomers us

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

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

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

241 In the oil structured using monoacylglycerol, MR was more effective than ER and RA.

242 dermis, sphingosine beta-hydroxyceramide and monoacylglycerol; mutants displayed decreased proportion

243 N-acylethanolamines, monoacylglycerols, N-acylamino acids, and N-acylneurotra

244 The oleogels were formed only at monoacylglycerol:native phytosterol (MAG:NPS) ratios of

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

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

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

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

249 reesterified into TG, primarily through the monoacylglycerol pathway.

250 sphosphatidic acid (LBPA), also known as bis-monoacylglycerol phosphate, either directly or via the L

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

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

253 obisphosphatidic acid (LBPA; also called bis(monoacylglycerol)phosphate) via treatment with its precu

254 and bis(monoacylglycerol)phosphate), whereas levels of OXPHOS me

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

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

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

258 delilla wax, fully hydrogenated palm oil and monoacylglycerols showed mechanical properties similar t

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

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

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

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

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

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

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

266 ransfer of acyl chains from TAGs to DAGs and monoacylglycerols to remodel the acyl chains of TAGs.

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

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

269 [3H]delta4Ach-containing diacylglycerol and monoacylglycerol were apparent along the time course of

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

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

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

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

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

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

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

277 ll previous crystallization trials have used monoacylglycerols, with 1-(cis-9-octadecanoyl)-rac-glyce

278 The operating conditions that optimized monoacylglycerol yields and oxidative stability were a g