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 (DGKs) convert DAG into phosphatidic acid, r

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

8 DAG theory is consistent with Weinberg's finding that ad

9 DAGs can also inform the data analysis strategy based on

10 DAGs encoding knowledge about the data-generating proces

11 DAGs help identify threats to causal inference such as c

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

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

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

15 y 50% after iv and po fat, membrane Di-C18:2 DAG species doubled after iv fat and correlated with PKC

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

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

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

19 sn-1,3 DAG is the preferred substrate for the consecutive hydro

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

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

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

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

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

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

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

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

28 mportant consequences when the ontology is a DAG-this is the case, for example, with the Gene Ontolog

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

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

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

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

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

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

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 Ala-DAG formation in Corynebacterium glutamicum is dependent

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

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

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

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

43 Ceramide and DAG content did not change.

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

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

46 ups from phospholipids and galactolipids and DAG:DAG transacylation.

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

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

49 ncreased the cellular content of both PA and DAG.

50 the disassociation of hepatic steatosis and DAG accumulation from hepatic insulin resistance in CGI-

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

52 gly correlated with hepatic triglyceride and DAG content, supporting a potential lipogenic role of PN

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

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

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

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

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

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

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

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

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

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

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

64 In particular, C-DAG provides a simple method for identifying amyloidogen

65 Thus, C-DAG provides a cell-based alternative to widely used in

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

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

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

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

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

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

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

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

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

75 DAG kinases (DGKs) convert DAG into phosphatidic acid, resulting in termination of

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

77 es allowed the estimation that this critical DAG content corresponds to about 1.9-2.5% of FFA, which

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

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

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

81 1,3 and sn-2,3, it suggests that TAG-derived DAG cannot directly enter phospholipid synthesis or acti

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

83 f triacylglycerides (TAG), diacylglycerides (DAG) and free fatty acids (FFA).

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

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

86 Diacylglycerol (DAG) produced after TCR stimulation functions as a secon

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

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

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

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

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

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

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

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

95 phosphatidylcholine (PC) and diacylglycerol (DAG), thus enriching PC-modified fatty acids in the DAG

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

97 ,5-trisphosphate (IP(3)) and diacylglycerol (DAG).

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

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

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

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

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

103 insic lipid kinase, favoring diacylglycerol (DAG) as a substrate and generating phosphatidic acid (PA

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

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

106 (TAG) hydrolysis, generating diacylglycerol (DAG) and fatty acids.

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

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

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

110 ocellular lipid-intermediate diacylglycerol (DAG).

111 mediated mechanism involving diacylglycerol (DAG) or phosphatidylinositol-4,5-bisphosphate (PIP(2)).

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

113 abolize the second messenger diacylglycerol (DAG) and limit Ras/ERK activation.

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

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

116 ty has been linked to muscle diacylglycerol (DAG) accumulation and insulin resistance.

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

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

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

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

121 condary to the generation of diacylglycerol (DAG) induced by LPS.

122 pathways: transacylation of diacylglycerol (DAG) with acyl groups from phospholipids and galactolipi

123 , phosphatidic acid (PA), or diacylglycerol (DAG), respectively.

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

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

126 A lipid product of PLC, diacylglycerol (DAG), and its metabolites, polyunsaturated fatty acids (

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

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

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

130 ellular lipids, specifically diacylglycerol (DAG).

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

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

133 rence (RNAi), we showed that diacylglycerol (DAG)-dependent PKCs triggered rate-limiting steps of lam

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

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

136 rsor-product relationship to diacylglycerol (DAG).

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

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

139 Arachidonic acid-containing diacylglycerols (DAG) activate protein kinase C (PKC), which promotes thr

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

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

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

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

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

145 Lard-based diacylglycerols (DAGs) were blended with lard in various concentrations (

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

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

148 in resistance was dependent on the different DAG isomers.

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

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

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

152 in insulin-sensitive, seemingly dissociating DAG from the development of insulin resistance.

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

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

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

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

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

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

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

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

161 ents confirmed that the formation of GE from DAG is extensive at temperatures above 230-240 degrees C

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

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

164 hierarchical structure established in the GO DAG.

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

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

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

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

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

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

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

172 Directed acyclic graphs (DAGs) were introduced into epidemiology several years la

173 Directed acyclic graphs (DAGs) were used to explore the structural basis for bias

174 S2 tyrosine phosphorylation, reduced hepatic DAG content, and reduced PKCepsilon activity.

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

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

177 However, DAG increased in lipid droplets or lipid-associated endo

178 However, it is not clear if DAG-promoted TRPV1 activation occurs independently from

179 ugh PC and enrich the hydroxy fatty acids in DAG, and thus in TAG.

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

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

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

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

184 es thrombosis, and DGKE normally inactivates DAG signaling.

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

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

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

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

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

190 (2+)]pm was prevented, the carbachol-induced DAG and PKC responses were somewhat reduced, but PKCbeta

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

192 Intravenously injected DAG peptide homes to neurovascular unit endothelial cell

193 necessary to control different intracellular DAG pools.

194 ntrast, [(14)C]glycerol most rapidly labeled DAG.

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

196 ings suggest that lipid accumulation (mainly DAGs), rather than the activation of JNK or IKK, is pivo

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

198 and a rise in distinct myocellular membrane DAG, while endotoxin-induced insulin resistance is exclu

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

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

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

202 oxidation leading to accumulation of muscle DAG does not necessarily lead to insulin resistance, as

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

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

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

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

207 rane-mimicking environment in the absence of DAG.

208 line as a tool to probe the accessibility of DAG generated in response to osmotic stress.

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 with either acidification or application of DAG analogs failed to activate the channels, whereas PUF

212 ortance of intracellular compartmentation of DAG in causing lipotoxicity and hepatic insulin resistan

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

214 tically manipulating the cellular content of DAG or PA.

215 Furthermore, conversion of DAG in the leaflets facing the chloroplast intermembrane

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

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

218 ls, which supports an individual function of DAG in each membrane leaflet.

219 In the present study, the impact of DAG content and temperature on the formation of GE using

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

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

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

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

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

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

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

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

228 that each line has an individual pattern of DAG, phosphatidic acid, phosphatidylcholine, and triacyl

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

230 Probing the steady-state pools of DAG and understanding how they contribute to the synthes

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

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

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

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

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

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

237 osphatidic acid, resulting in termination of DAG signaling.

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

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

240 ed in the blends with high concentrations of DAGs.

241 owards higher temperatures as the content of DAGs increased above 50%.

242 In general, the effects of DAGs were found to be dependent on concentration.

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

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

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

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

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

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

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

250 -30 Galphaq and egl-8 PLCbeta) that produces DAG, and by DAG binding to short and long UNC-13 protein

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

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

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

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

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

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

257 tion consistency for high dimensional sparse DAGs is established.

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

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

260 through the enzymatic reactions that supply DAG.

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

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

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 hus enriching PC-modified fatty acids in the DAG pool prior to forming TAG.

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 ion of GE accelerates in particular when the DAG levels in refined oils exceed 3-4% of total lipids.

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

283 Thoughtful DAG analyses require clear research questions but are ea

284 C. elegans expresses three DAG-regulated PKCs, and blocking UNC-18 Ser322 phosphory

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

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

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

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

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

290 PA and a decreased cellular content of total DAG.

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

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

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

294 e authors now revisit Weinberg's paper using DAGs to represent scenarios that arise from her original

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

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

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

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