ライフサイエンスコーパス: DAG

1 DAG (0-2.5wt%) had little effect on the chemical stabili

2 DAG activated TRP even in the presence of a DAG-lipase i

3 DAG also caused an overall decrease in diphenylhexatrien

4 DAG and IP(3) each control diverse cellular processes an

5 DAG content of 5% and 10% resulted in lowering of the of

6 DAG kinases and phospholipase D, the enzymes that produc

7 DAG may potentially be used as a tool to enhance deliver

8 DAG-MRI and PET/CT have similar success in the different

9 DAGs can also inform the data analysis strategy based on

10 DAGs help identify threats to causal inference such as c

11 nd 41% TAG with a stoichiometry of 27 PL, 10 DAG, and 23 TAG molecules per apoB:1000.

12 teins; these particles contained 46% PL, 13% DAG, and 41% TAG with a stoichiometry of 27 PL, 10 DAG,

13 O mice accumulated sn-1,3 DAG and not sn-1,2 DAG.

14 hile the levels of CPA increased in PC-sn-2, DAG-sn-1 and DAG-sn-2, and both sn-1/3 and sn-2 position

15 tains 84% of DAG (66% of 1,3-DAG, 18% of 1,2-DAG) and 16% of triacylglycerol (TAG) along with micro n

16 dental research was first advocated in 2002, DAGs have yet to be widely adopted in this field.

17 revealed that HSL KO mice accumulated sn-1,3 DAG and not sn-1,2 DAG.

18 l muscle and that the accumulation of sn-1,3 DAG originating from lipolysis does not inhibit insulin-

19 The accumulated DAG was sn-1,3 DAG, which is known not to activate PKC, and insulin sig

20 DAG-rich oil contains 84% of DAG (66% of 1,3-DAG, 18% of 1,2-DAG) and 16% of triacylglycerol (TAG) al

21 We conclude that 1,3-DAG-rich oil is a low calorie fat and exhibits hypolipid

22 lesterol and TAG levels in rats fed with 1,3-DAG-rich oil were found to be significantly reduced as c

23 cerol (TAG) with a stoichiometry of 46 PL, 6 DAG, and 15 TAG molecules per apoB:1000.

24 001) when the blends contained more than 60% DAGs.

25 PMA and AJH-836 (a DAG-mimetic that preferentially activates PKCepsilon) pr

26 ntly led to the identification of AJH-836, a DAG-lactone with preferential affinity for novel isozyme

27 -myristate 13-acetate (PMA), which acts as a DAG mimetic.

28 DAG activated TRP even in the presence of a DAG-lipase inhibitor, inconsistent with a requirement of

29 Altogether, we present a DAG-mediated activation mechanism for TRPC4/5 channels t

30 (DAG), polyunsaturated fatty acids (PUFAs, a DAG metabolite), phosphatidylinositol bisphosphate (PIP2

31 its PKC-dependent phosphorylation, abolishes DAG-induced potentiation of synaptic transmission in hip

32 sion of diacylglycerol kinase beta abrogated DAG accumulation at the phagosome, leading to impaired r

33 The accumulated DAG was sn-1,3 DAG, which is known not to activate PKC,

34 odorized oils in EVOO: R1 (10 x free acidity/DAG(exp)) >= 0.23 and R2 (DAG(exp)-DAG(theor)) < 0, in g

35 n agreement with the values of free acidity; DAG types found were in agreement with the representativ

36 ), sphingolipids, di- and tri-acylglycerols (DAGs and TAGs), and sterol derivatives.

37 actionation of subcellular membranes affects DAG pools.

38 genotype and exercise on BChE activity, AG, DAG, and energy intake are unknown.

39 r baseline BChE activity, higher baseline AG:DAG ratio, attenuated AG suppression after a fixed meal,

40 04); however, exercise lowered AG and the AG:DAG ratio to a greater extent in AAs (P <= 0.023), offse

41 ases BChE activity, suppresses AG and the AG:DAG ratio, and corrects the higher AG profile observed i

42 Ala-DAG formation in Corynebacterium glutamicum is dependent

43 alanylated lipid, Alanyl-diacylglycerol (Ala-DAG).

44 The alignment DAG provides a natural way to represent a distribution i

45 for identification and quantification of all DAG species including regioisomers, particularly in an a

46 ls of CPA increased in PC-sn-2, DAG-sn-1 and DAG-sn-2, and both sn-1/3 and sn-2 positions in TAG.

47 ein-2 (RASGRP2) gene coding for calcium- and DAG-regulated guanine exchange factor-1 (CalDAG-GEFI).

48 identified (opioid receptor and PKA/CREB and DAG/IP3 signalling pathways) are genetically associated

49 and their downstream effectors PKA/CREB and DAG/IP3.

50 PA phosphatase controls the levels of PA and DAG for the synthesis of triacylglycerol and membrane ph

51 ission, we find that shorter forms of PA and DAG promote the vesiculation ability of COPI fission fac

52 fic DAG-kinase-1, which interconverts PA and DAG, and whose depletion impairs egress and causes paras

53 ncreased the cellular content of both PA and DAG.

54 and transcriptional networks between PMA and DAG-lactones.

55 in resistance by suppressing hepatic TAG and DAG accumulation through enhanced mitochondrial carbohyd

56 Blending of TAGs and DAGs may serve as a solution to achieve specific functio

57 d mediators modulate rice root architecture; DAG promotes LR formation and suppresses SR growth where

58 However, traditional methods of assaying DAG pools are difficult, because its abundance is low an

59 LCgamma to generate DAG but rely on baseline DAG levels instead.

60 Here we show that a delicate balance between DAG and its downstream product, phosphatidic acid (PA),

61 low glucose condition; the crosstalk between DAG and PKC regulates the span of anabolic bistable regi

62 to generate phosphatidic acid (PA), and both DAG and PA are lipid mediators in the cell.

63 e protein kinase C (PKC) can be activated by DAG and promotes receptor desensitization, we also exami

64 and egl-8 PLCbeta) that produces DAG, and by DAG binding to short and long UNC-13 proteins.

65 TRP was opened by DAG and silenced by ATP, suggesting DAG-kinase (DGK) inv

66 At 22 degrees C, DAG at 33 mol % increased PI-PLC activity in all of the

67 hosphatidylcholine bilayers at 22 degrees C, DAG induced/increased enzyme binding and activation, but

68 C-DAG relies on the natural ability of Escherichia coli ce

69 called curli-dependent amyloid generator (C-DAG).

70 The kinetics of [(14)C]-DAG and [(14)C]-TAG accumulation and the regiospecificit

71 We identified a cyclic peptide, CDAGRKQKC (DAG), that accumulates in the hippocampus of hAPP-J20 mi

72 ryotes and eukaryotes, being produced by CDP-DAG synthase (CDS).

73 Cytidine diphosphate diacylglycerol (CDP-DAG) is a central lipid intermediate for several pathway

74 the cytidine diphosphate diacylglycerol (CDP-DAG) pathway, is avirulent in the mouse model of systemi

75 osphate synthase is not synthesized from CDP-DAG, as was previously thought.

76 ed the ER and Golgi, probably to provide CDP-DAG for the phosphatidylinositol synthases.

77 is thaliana) that target an Escherichia coli DAG kinase (DAGK) to each leaflet of each chloroplast en

78 dystrophin-associated glycoprotein complex (DAG) has been clinically challenging.

79 n the C-terminal PDZ-binding motif conferred DAG sensitivity to the channel.

80 kinase (Dgk) zeta, an enzyme which converts DAG into phosphatidic acid, limits inflammatory cytokine

81 ded when phagosomes fail to reach a critical DAG concentration.

82 We also showed that exogenously delivered DAG homes to the brain in mouse models of glioblastoma,

83 a1 controls OC numbers via a CSF-1-dependent DAG/beta-catenin/cyclinD1 pathway.

84 4)C]glycerol studies demonstrated PC-derived DAG is the major source of DAG for TAG synthesis in both

85 and larger bulk phosphatidylcholine-derived DAG pool that is more slowly turned over for TAG biosynt

86 rapidly produced phosphatidylcholine-derived DAG pool.

87 ork, we examined the phosphorylation of Dgk1 DAG kinase by casein kinase II (CKII).

88 es and highlight a potential role of Dgkzeta-DAG/phosphatidic acid axis as a modulator of inflammator

89 Diacylglycerol (DAG) and Protein-kinase C (PKC) signaling in the nerve t

90 Diacylglycerol (DAG) is an intermediate in metabolism of both triacylgly

91 Diacylglycerol (DAG), levels of which are tightly regulated by diacylgly

92 Diacylglycerol (DAG), the lipid product of PLC that activates convention

93 Diacylglycerol (DAG), the product of the PLC-catalyzed PI(4,5)P(2) hydro

94 Diacylglycerol (DAG), which is also increased in muscle exposed to high

95 Diacylglycerol (DAG)-induced activation of phosphatidylinositol-phosphol

96 Diacylglycerol (DAG)/phorbol ester-regulated protein kinase C (PKC) isoz

97 tocytes contained 69% PL, 9% diacylglycerol (DAG), and 23% triacylglycerol (TAG) with a stoichiometry

98 ic triacylglycerol (TAG) and diacylglycerol (DAG) content was significantly attenuated with DPP-4 inh

99 expression, and ceramide and diacylglycerol (DAG) content were measured in muscle from a group of obe

100 uscle triglyceride (TAG) and diacylglycerol (DAG) content, which was associated with increased PKCeps

101 Phosphatidic acid (PA) and diacylglycerol (DAG) have been found previously to be required for the f

102 h monoacylglycerol (MAG) and diacylglycerol (DAG) to generate DAG and TAG, respectively.

103 Ca(2+)- and diacylglycerol (DAG)-activated protein kinase C (cPKC) promotes learning

104 itol 1,4,5-trisphosphate and diacylglycerol (DAG).

105 he site of CPA biosynthesis, diacylglycerol (DAG), and TAG.

106 based on the fact that both diacylglycerol (DAG) and free fatty acids are not interdependent after m

107 recruited to the membrane by diacylglycerol (DAG) in a phospholipase C-gamma (PLCgamma)-dependent man

108 In contrast, diacylglycerol (DAG) was not generated uniformly across the phagosomal p

109 rease in total and cytosolic diacylglycerol (DAG) content that was temporally associated with protein

110 ccharomyces cerevisiae, Dgk1 diacylglycerol (DAG) kinase catalyzes the CTP-dependent phosphorylation

111 ontaining multiple different diacylglycerol (DAG) and acyl donor substrate pools.

112 As TAG is produced from diacylglycerol (DAG), successful engineering strategies to enhance TAG l

113 rtrophic stimuli to generate diacylglycerol (DAG) from PI4P in the Golgi apparatus, in close proximit

114 licated increases in hepatic diacylglycerol (DAG) content leading to activation of novel protein kina

115 ely 50% reduction in hepatic diacylglycerol (DAG) content, an approximately 80% reduction in hepatic

116 as increased hepatocellular diacylglycerol (DAG) content, a well-documented trigger of insulin resis

117 ocellular lipid-intermediate diacylglycerol (DAG).

118 One of these lipids-diacylglycerol (DAG)-rapidly accumulates in a broad domain that overlaps

119 g the lipid second messenger diacylglycerol (DAG) and subsequent phosphorylation of its activation lo

120 r the lipid second messenger diacylglycerol (DAG) and the phorbol ester tumor promoters.

121 ne-embedded second messenger diacylglycerol (DAG) through its interactions with the C1 regulatory dom

122 erates the second messengers diacylglycerol (DAG) and IP3 and ultimately results in microneme secreti

123 Moreover, diacylglycerol (DAG) acts after PA in late fission, with this role of DA

124 In muscle, diacylglycerol (DAG) and intramyocellular triacylglycerol were increased

125 we determined the effect of diacylglycerol (DAG) and monoacylglycerol (MAG) on the oxidative stabili

126 s shows a marked increase of diacylglycerol (DAG) and phosphatidic acid, the precursors for TAG, in t

127 creases the concentration of diacylglycerol (DAG) and the activity of DAG kinases (DGKs) in membranou

128 we demonstrate that loss of diacylglycerol (DAG) kinase (Dgk) zeta, an enzyme which converts DAG int

129 n (Fld1), and a regulator of diacylglycerol (DAG) production, Nem1.

130 rmacological manipulation of diacylglycerol (DAG), and protein kinase D (PKD) activity, activated or

131 ed with their Ca(2+)- and/or diacylglycerol (DAG)-dependent translocation to the plasma membrane.

132 hat DGKeta can phosphorylate diacylglycerol (DAG) with different acyl side chains (8:0, 12:0, 18:1).

133 kinase (DGK) phosphorylates diacylglycerol (DAG) to generate phosphatidic acid (PA), and both DAG an

134 sphatidylglycerol to produce diacylglycerol (DAG), dihydroxyacetone, and orthophosphate.

135 PC channels, the PLC product diacylglycerol (DAG) is not sufficient for channel activation, whereas T

136 ts not being due to reducing diacylglycerol (DAG) or IP3 availability, i.e. PIP2 modulation of AHPs i

137 KC isoform involved requires diacylglycerol (DAG) but is Ca(2+) -insensitive, which are characteristi

138 It is converted to substrate diacylglycerol (DAG) for MGDG Synthase (MGD1) which adds to it a galacto

139 rsial evidence has suggested diacylglycerol (DAG), polyunsaturated fatty acids (PUFAs, a DAG metaboli

140 f triacylglycerol synthesis: diacylglycerol (DAG), which may cause insulin resistance in liver by act

141 re, we report that targeting diacylglycerol (DAG) kinase zeta (DGKzeta), a negative regulator of DAG-

142 resynaptic activation of the diacylglycerol (DAG)/protein kinase C (PKC) pathway is a central event i

143 ipid species belonged to the diacylglycerol (DAG, 17 species) and triacylglycerol (TAG, 17 species) c

144 line units from Lip to yield diacylglycerol (DAG) and phosphocholine (PC) products, leading to the de

145 a nutritionally enriched 1,3-diacylglycerol(DAG)-rich oil from a blend of refined sunflower and rice

146 receptor-4, accumulation of diacylglycerols (DAG)/ceramides, and activation of protein kinase C (PKC)

147 of this work was to produce diacylglycerols (DAG) and monoacylglycerols (MAG) with a high content of

148 ion of triglycerides, toxic diacylglycerols (DAG) and ceramides or suppress muscle PKCepsilon sarcole

149 Diacylglycerols (DAGs) are important intermediates of lipid metabolism an

150 lipids, acylated MGDGs, and diacylglycerols (DAGs), the direct precursor of TAGs, was observed.

151 The total amount of diacylglycerols (DAGs) was in agreement with the values of free acidity;

152 minated the accumulation of diacylglycerols (DAGs), which is known to have an impact on insulin signa

153 in resistance was dependent on the different DAG isomers.

154 gain insight into the origin of differential DAG affinities, we conducted high-resolution NMR studies

155 ible, at least in part, for the differential DAG affinities.

156 imer's disease dataset in which differential DAGs are identified between cases and controls.

157 ([Ca(2+)]pm), with additional effect during DAG spikes.

158 ation, we turned to its downstream effector, DAG.

159 in a cuvette are not sufficient to elucidate DAG effects that take place at the domain level.

160 actions with membrane-mimicking environment, DAG, and phosphatidylserine, as well as the affinities a

161 acting downstream of the two other essential DAG/PKC substrates, Munc13-1 and Munc18-1.

162 e acidity/DAG(exp)) >= 0.23 and R2 (DAG(exp)-DAG(theor)) < 0, in genuine EVOO.

163 es, Munc13-1 and Munc18-1, are essential for DAG-induced potentiation of vesicle priming, but the rol

164 he C terminus of TRPC5 as a prerequisite for DAG sensitivity.

165 together, these data support a key role for DAG activation of PKCtheta in the pathogenesis of lipid-

166 l (MAG) and diacylglycerol (DAG) to generate DAG and TAG, respectively.

167 on acute activation of PLCgamma to generate DAG but rely on baseline DAG levels instead.

168 se (BChE) hydrolyzes AG to des-acyl-ghrelin (DAG), potentially decreasing appetite.

169 hierarchical structure established in the GO DAG.

170 ing of GO-terms, (III) mapping to reduced GO-DAGs including visualization capabilities and (IV) prior

171 hat ontologies are a directed acyclic graph (DAG) of terms and hierarchical relations, algorithms are

172 pled alignments as a directed acyclic graph (DAG) whose nodes are alignment columns; each path throug

173 y take the form of a directed acyclic graph (DAG).

174 s and tools such as directed acyclic graphs (DAGs) and Bayesian statistical techniques can provide im

175 ted organization as directed acyclic graphs (DAGs) and the lack of tools allowing to exploit this str

176 Directed acyclic graphs (DAGs) are nonparametric graphical tools used to depict c

177 alence class of the directed acyclic graphs (DAGs) in a genetical genomics analysis framework.

178 are represented as directed acyclic graphs (DAGs) of collections of 'selectivity' relations, where a

179 Little is known about how DAG kinase activity is regulated by posttranslational mo

180 We illustrate how DAGs can be used to identify 1) potential confounders, 2

181 These subdomains become enriched in DAG.

182 duced only a small and transient increase in DAG levels, unlike the robust and more sustained increas

183 To determine whether increases in DAG and PA impair insulin signaling when produced by pat

184 ressing cells showed a 7.7-fold reduction in DAG kinase activity; the reduced enzyme activity could b

185 of bioactive lipids, including elevations in DAGs and reductions in endocannabinoids and eicosanoids.

186 A lipid extract enriched in DAGs from wild-type cells initiates development and lipi

187 Increased DAG and decreased PC levels were examined through the ki

188 We found that, despite an increased DAG content in muscle after exercise in HSL KO mice, the

189 ng the DAG kinase zeta, which have increased DAG levels, we demonstrate that DAG modulates CSF-1-depe

190 Paradoxically, increasing DAG kinase activity can enhance the robustness of DAG/ac

191 pendent phosphorylation and PKC-independent, DAG-mediated membrane recruitment, possibly explaining t

192 great efforts on the analysis of individual DAG species have recently been made by utilizing mass sp

193 (2+)]pm was prevented, the carbachol-induced DAG and PKC responses were somewhat reduced, but PKCbeta

194 We conclude that exocytosis-induced DAG spikes efficiently recruit both conventional and nov

195 Intravenously injected DAG peptide homes to neurovascular unit endothelial cell

196 necessary to control different intracellular DAG pools.

197 tical perspective of GO as manifested by its DAG-structure and the containing hierarchy levels for cu

198 -6,657,983) and asthma phenotypes (Lifelines/DAG [Dutch Asthma GWAS]/GASP [Genetics of Asthma Severit

199 insulin granules evokes brief (<10 s) local DAG elevations ("spiking") at the plasma membrane becaus

200 resistance involves diacylglycerol-mediated (DAG-mediated) activation of protein kinase C-epsilon (PK

201 -induced PKC translocation entirely mirrored DAG spiking, whereas PKCbetaI translocation showed a sus

202 In PI/galactosylceramide mixtures, DAG may exert its activation role through the generation

203 Similar associations between muscle DAG content, PKCtheta activation, and muscle insulin res

204 emoved (Syt1(Delta109-116)), supports normal DAG-induced potentiation.

205 These data suggest that PA, but not DAG, is associated with impaired insulin action in mouse

206 tion of PC, but the sn-1 position of de novo DAG and indicated similar rates of nascent acyl groups i

207 The resultant DAG-rich oil contains 84% of DAG (66% of 1,3-DAG, 18% of 1,2-DAG) and 16% of triacylg

208 rane-mimicking environment in the absence of DAG.

209 of diacylglycerol (DAG) and the activity of DAG kinases (DGKs) in membranous structures.

210 The addition of DAG did not cause an appreciable change in the interfaci

211 Analysis of the cellular compartmentation of DAG revealed that DAG increased in the membrane fraction

212 tically manipulating the cellular content of DAG or PA.

213 TAG levels have focused on the conversion of DAG to TAG.

214 tography/mass-spectrometry determinations of DAG and PUFAs in membranes enriched in rhabdomere obtain

215 ymes and that the latter limits formation of DAG and negatively regulates TRPV1 channel activity.

216 We also examined the influence of DAG and MAG on the physical properties of SSO.

217 Conversely, pharmacological inhibition of DAG kinases or expression of an inactive diacylglycerol

218 sults emphasize that the interconversions of DAG and PC pools can impact oil production and compositi

219 DGK inhibitor R59022 increased the level of DAG and decreased PA, which also restored the root pheno

220 It is well-known that the mass levels of DAG are altered under disease states.

221 mical structure and cellular localization of DAG in skeletal muscle revealed that HSL KO mice accumul

222 mical structure and cellular localization of DAG into account when evaluating the role of DAG in lipi

223 Modulation of DAG levels suggested that NOX activation is precluded wh

224 presence of DAG-generated nanodomains, or of DAG-induced lipid packing defects, is proposed instead f

225 talyzes the CTP-dependent phosphorylation of DAG to form phosphatidic acid (PA).

226 The presence of DAG-generated nanodomains, or of DAG-induced lipid packi

227 or PKD activation in which the production of DAG leads to the local accumulation of PKD at the membra

228 The physical properties of DAG and MAG in the SSO may be related to the chemical st

229 nase beta mutant increased the proportion of DAG-positive phagosomes, concomitantly potentiating phag

230 nase zeta (DGKzeta), a negative regulator of DAG-mediated cell signaling, protected against allergic

231 inase activity can enhance the robustness of DAG/active PKC polarization with respect to chemoattract

232 after PA in late fission, with this role of DAG also requiring shorter acyl chains.

233 DAG into account when evaluating the role of DAG in lipid-induced insulin resistance in skeletal musc

234 trated PC-derived DAG is the major source of DAG for TAG synthesis in both tissues.

235 he stationary phase-dependent stimulation of DAG kinase activity.

236 Supplementation of DAG to OsDGK1-overexpressing seedlings restored the LR d

237 ll exercise to stimulate the accumulation of DAGs in skeletal muscle.

238 Therefore, quantitative analysis of DAGs in biological samples can provide critical informat

239 vestigated whether the described function of DAGs as mediators of lipid-induced insulin resistance wa

240 Finally, we discuss the usefulness of DAGs during study design, subject selection, and choosin

241 For example, one DAG shows that statistical adjustment for the pressure p

242 CLC) cells revealed that PKCepsilon or other DAG-regulated PKCs (PKCalpha and PKCdelta) were dispensa

243 esis through activation of mTOR via PLCgamma/DAG/PKC signaling, not via Akt/Rheb signaling.

244 nce of PLCgamma1 are normalized in PLCgamma1/DAG kinase zeta double null cells.

245 tations in Munc13-1 or Munc18-1 that prevent DAG-induced potentiation, the synaptotagmin-1 mutation d

246 To manipulate and probe DAG pools in an in vivo context, we generated multiple s

247 -30 Galphaq and egl-8 PLCbeta) that produces DAG, and by DAG binding to short and long UNC-13 protein

248 hod for directly identifying and quantifying DAG species including regioisomers present in lipid extr

249 (10 x free acidity/DAG(exp)) >= 0.23 and R2 (DAG(exp)-DAG(theor)) < 0, in genuine EVOO.

250 ting fatty acid synthesis, which both reduce DAG levels.

251 gl-30 Galphaq and egl-8 PLCbeta and requires DAG binding to UNC-13L (but not UNC-13S).

252 The resultant DAG-rich oil contains 84% of DAG (66% of 1,3-DAG, 18% of

253 otably, ERRgamma did not restore sarcolemmal DAG complex, which is thus dispensable for antidystrophi

254 eyes showed light-dependent increment in six DAG species and no changes in PUFAs.

255 tion consistency for high dimensional sparse DAGs is established.

256 ng this balance is the apicomplexan-specific DAG-kinase-1, which interconverts PA and DAG, and whose

257 OsDGK1 led to a decline in the DGK substrate DAG whereas specific PA species decreased in dgk1 roots.

258 pened by DAG and silenced by ATP, suggesting DAG-kinase (DGK) involvement.

259 through the enzymatic reactions that supply DAG.

260 The results strongly support DAG as the endogenous TRP agonist, as some of its verteb

261 For TAG synthesis, DAG requires a fatty acid from the acyl-CoA pool or phos

262 wed two main clusters describing the system, DAG lipids and phenyllactic acid.

263 regulators of ion channel activity and that DAG sensitivity is a distinctive hallmark of TRPC channe

264 ve increased DAG levels, we demonstrate that DAG modulates CSF-1-dependent proliferation and beta-cat

265 Given that DAG appears in different stereoisomers and has different

266 The above data reinforce the idea that DAG functions as an important physical agent in regulati

267 nding to the various domains, indicated that DAG activates PI-PLC whenever it can generate fluid doma

268 llular compartmentation of DAG revealed that DAG increased in the membrane fraction of high fat-fed m

269 X-ray scattering (WAXS) analysis showed that DAG did not alter the structured organisation of SSO, wh

270 The DSC thermograms showed that DAGs changed the melting and crystallisation profiles of

271 The DAG-PKC hypothesis can explain the occurrence of hepatic

272 lly informative for T2D pathogenesis; b) the DAG and TAG lipid classes partially share genetic basis

273 DAGK inhibition substantially increased the DAG signal evoked by TRPV1 activation but not that evoke

274 point increased (P<0.05) with increasing the DAG concentrations (10-100%).

275 By utilizing cells lacking the DAG kinase zeta, which have increased DAG levels, we dem

276 Formation of the DAG domain is required for Cdc42 and Rho activation and

277 AD and in mouse models, as the target of the DAG peptide.

278 The calorific value of the DAG-rich oil was estimated to be 6.45Kcals/g as against

279 Nutritional studies of the DAG-rich oil were conducted in Wistar rats and compared

280 PLCgamma pathway activates mTOR through the DAG/PKC signaling branch, independent of the conventiona

281 re alignment columns; each path through this DAG then represents a valid alignment.

282 The affinity of C1 domains to DAG varies considerably among PKCs.

283 es more efficient movement of CPA from PC to DAG and establishes LcPDCT as a useful factor to combine

284 r of the phosphocholine headgroup from PC to DAG.

285 her the conversion of phosphatidylcholine to DAG impacts TAG levels in seeds.

286 shown to render C1Bdelta less responsive to DAG and thereby emulate the behavior of C1B domains from

287 ntent of total PA, without a change in total DAG.

288 hod, we revealed a 16-fold increase of total DAG mass in the livers of ob/ob mice compared to their w

289 PA and a decreased cellular content of total DAG.

290 on of the concentration of triacylglycerols, DAG, MAG and free fatty acids (FFA) and the concentratio

291 Glucose stimulation of MIN6 cells triggered DAG spiking with concomitant repetitive translocation of

292 Two DAG targets, protein kinase C (PKC) beta and eta, are re

293 ted PKD activation loop phosphorylation upon DAG production.

294 +) -store release, or channel modulation via DAG and protein kinase C (PKC).

295 was significantly (P<0.0001) decreased when DAGs were added to the lard from 5-50%, whereas the DP w

296 ignaling biosensors, we investigated whether DAG spiking causes membrane recruitment of PKCs and whet

297 upled receptors, but it is not known whether DAG modulates TRPV1 during desensitization.

298 mum (7mol%) at lower water activities, while DAG content was favored at higher water activities (35mo

299 Interference with DAG spiking by purinoceptor inhibition prevented intermi

300 he compositions under study, with or without DAG, and quantitative evaluation of the phase behavior u