ライフサイエンスコーパス: LPC

1 LPC and/or biliary cells generated 0.78% and 2.45% of he

2 LPC C26:0 added to ABCD1-deficient microglia in culture

3 LPC is the major substrate of the secreted lysophospholi

4 LPC markers correlate positively with severity of liver

5 LPC markers were assessed by real-time polymerase chain

6 LPC or biliary cells terminally differentiate into funct

7 LPC transport requires lysophosphatidylcholine acyltrans

8 LPC transport via Mfsd2a has been shown to be necessary

9 LPC treatment of PMH or Huh7 cells induced release of EV

10 LPC-activated inflammasome also requires ASC (apoptotic

11 LPCs have intrinsic, cell proliferation-independent char

12 ce Them1 catalysis of acyl-CoA, whereas 18:1 LPC destabilizes and inhibits activity, which we verify

13 holipids lysophosphatidylcholine (LPC) 18:1, LPC 16:0, and 9,10-EpOME in oxaliplatin-induced acute pa

14 tarch suspensions (9% w/w) containing 0.5-5% LPC were subjected to hydrolysis by porcine pancreatic a

15 mediated by direct 12-LOX oxidation of 2-AA-LPC and 2-AA-LPE.

16 ses in the initial rate of radiolabeled 2-AA-LPC and arachidonic acid (AA) production, respectively,

17 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) and 2-arachidonoyl-lysophosphatidylethanolamine (2-

18 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC) from 1-palmitoyl-2-[(14)C]arachidonoyl-sn-glycero-3

19 2-arachidonoyl-lysophosphatidylcholine (2-AA-LPC).

20 ed the calcium-stimulated production of 2-AA-LPC, 2-AA-LPE, and 12-HETE-lysophospholipids in mouse pl

21 reover, we observed robust increases in 2-AA-LPC, 2-AA-LPE, and their downstream 12-LOX oxidation pro

22 a revealed the robust production of AA, 2-AA-LPC, and 2-docosahexaenoyl-LPC that was over 10-fold gre

23 ssels, showed that luminal but not abluminal LPC potently induced permeability, and that this require

24 2-Acyl LPC from water fraction after precipitation in cold (-20

25 2-Acyl-lysophosphatidylcholine (2-acyl LPC), fatty acids ethyl esters (FAEEs) and free fatty ac

26 Fetal and adult LPCs had significantly greater reprogramming efficiency

27 protein (RFP)-tagged EV marker, CD63, after LPC treatment of cotransfected Huh-7 cells.

28 astrocyte-specific Fpn knock-out mice after LPC-induced demyelination.

29 on a molecular level, influenced by amylose-LPC complexation; however the effect depends on the dige

30 lly form distinct inflammasomes, activate an LPC-induced inflammasome and are important in astroglios

31 m to support mouse biliary-derived DRs as an LPC pool to replenish hepatocytes in a quantitatively re

32 ed myelin repair therapy was conducted in an LPC rat model using a mesenchymal stem cell-based hepato

33 Importantly, LPC 18:1 and LPC 16:0 can induce Ca(2+) transients in primary sensory

34 ipids lysophosphatidylcholine (LPC) 18:1 and LPC 16:0 were significantly increased 24 h after oxalipl

35 the distinctive network dynamics in ACC and LPC during normal and pathological brain states.SIGNIFIC

36 Gpc1 and Ale1 are the major cellular GPC and LPC acyltransferases, respectively.

37 rs together with the induction of injury and LPC proliferation.

38 rall, switched words elicited larger LAN and LPC amplitude than non-switched words.

39 However, the LPA and LPC species that increase in BAL of bleomycin-injured mi

40 produces lysophosphatidylcholine (LPC), and LPC can be converted to PC by the lysophospholipid acylt

41 ntributors to the difference in both LPE and LPC levels.

42 can contribute to the differences in LPE and LPC.

43 levels of phosphatidylethanolamine, LPE, and LPC in the cells.

44 cyltransferase function but exhibits MAG and LPC hydrolase activities.

45 presence of two separate substrate (MAG and LPC)-binding sites in a single polypeptide.

46 te populations of neurons within the VTC and LPC during the visual processing of numerals and the per

47 ce of math-selective hubs within the VTC and LPC, we report here a remarkable heterogeneity of neural

48 information (face vs scene) in both VTC and LPC.

49 stablish a link between transport of DHA and LPCs by MFSD2A and human brain growth and function, pres

50 mokine expression localized to CK7(+) DR and LPCs in CFLD liver biopsies.

51 Primary cultures of hepatocytes and LPCs from AlfpCre(+)Trp53(Delta2-10/Delta2-10) mice, but

52 esigning particle shape based on anticipated LPC-NPPs.

53 nce of the tetratic order on alpha, we apply LPC-NPP analysis to other hard kites for 54 degrees <= a

54 nd key events in DR evolution were assessed: LPC proliferation, LPC biliary differentiation, and hepa

55 ear conditions in a flow chamber, LPA or ATX/LPC strongly enhances TEM of integrin-arrested T cells a

56 6% of the total, whereas the predominant BAL LPC species contained shorter chain, saturated acyl grou

57 liver parenchymal cells (LPCs; IKKalpha/beta(LPC-KO) ) were intercrossed with RIPK1(LPC-KO) or RIPK3(

58 ith a substrate-product relationship between LPC and LPA in pulmonary fibrosis.

59 t this type II NKT TCR binds with CD1d-bound LPC with micromolar affinities similar to that for sulfa

60 on of disease associated with aberrant brain LPC transport in humans.

61 Repopulation efficiency by LPC and/or biliary cells increased when extracellular ma

62 n and was prevented by LPC or OA, but not by LPC+OA.

63 usion channel formation and was prevented by LPC or OA, but not by LPC+OA.

64 The iNKT TCR CDR loop footprint on CD1d-LPC is anchored by the conserved positioning of the CDR3

65 of the LPC headgroup but stabilizes the CD1d-LPC complex in a closed conformation.

66 iferation of STAT3-deficient EpCAM(+)CD45(-) LPCs.

67 epithelial cell adhesion molecule(+)CD45(-) LPCs isolated from DDC-fed wild-type mice.

68 We studied mice with liver parenchymal cell (LPC)-specific disruption of the cylindromatosis (CYLD) l

69 easy and reproducible liver progenitor cell (LPC) isolation strategy based on aldehyde dehydrogenase

70 and the expression of liver progenitor cell (LPC) markers.

71 garding the extent of liver progenitor cell (LPC) proliferation in AH.

72 Liver progenitor cell (LPC)-enriched cell fractions were isolated from adult (6

73 ice lacking NEMO in liver parenchymal cells (LPC) spontaneously develop steatohepatitis and hepatocel

74 have indicated that liver progenitor cells (LPC) could give rise to hepatic epithelial cells during

75 ized by expansion of liver progenitor cells (LPC), which correlates with disease severity.

76 er RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice wi

77 tic IKK activity in liver parenchymal cells (LPCs; IKKalpha/beta(LPC-KO) ) were intercrossed with RIP

78 gulation of VDUP1 in lamina precursor cells (LPCs) coincided with the arrival of retinal axons into t

79 cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species

80 onogenic capacity of liver progenitor cells (LPCs) and hepatocytes.

81 Liver progenitor cells (LPCs) are necessary for repair in chronic liver disease

82 cells (LSCs) and leukemia progenitor cells (LPCs) displaying innate and acquired resistance, respect

83 contain bipotential liver progenitor cells (LPCs) that serve as an emergency cell pool to regenerate

84 ved in DR induction, liver progenitor cells (LPCs) were treated with taurocholate, and key events in

85 isolation of primary liver progenitor cells (LPCs), directed hepatocyte differentiation of primary LP

86 roliferation of liver stem/progenitor cells (LPCs), which can differentiate into hepatocytes or bilia

87 dult hepatocytes and liver progenitor cells (LPCs).

88 ial cells (BECs), or liver progenitor cells (LPCs).

89 patient-derived leukemia-propagating cells (LPCs) in murine xenografts.

90 ough hydrolysis of lysophosphatidyl choline (LPC).

91 OX9 proteins, the number of primary cilia(+) LPCs, and increased active gamma-glutamyltranspeptidase

92 d bilayer coating and are named Lipid-Pt-Cl (LPC) NPs, which showed significant antitumor activity bo

93 at complete NF-kappaB inhibition by combined LPC-specific ablation of RelA, c-Rel, and RelB did not p

94 We found that late positive complex (LPC) significantly increased when subjects accepted gamb

95 ated with an enhanced late positive complex (LPC, 500-800ms) largest on frontal sites.

96 vity (FRN), and the late positive component (LPC), indicate that social comparison manifests in three

97 LAN - followed by a Late Positive Component (LPC).

98 hyl-allo-threonyl hydroxamate-based compound LPC-058 is a potent inhibitor of UDP-3-O-(R-3-hydroxymyr

99 By contrast, LPC did not contribute to hepatocyte regeneration during

100 Contrastingly, LPC promotes RPT aggregation at both submicellar and mic

101 og (Hh) is a signal well known to coordinate LPC proliferation and differentiation in response to ret

102 in areas within the lateral parietal cortex (LPC) and ventral temporal cortex (VTC) have been shown t

103 creased activity in lateral parietal cortex (LPC)--"retrieval success effects" that are thought to ge

104 rain (Deltad/d) and lattice plane curvature (LPC) for 150 mm diameter wafers.

105 del to study the behavior of patient-derived LPC clones, which provides insights relevant for experim

106 monstrate that pluripotent stem cell-derived LPCs choose hepatic fate when cultured next to healthy h

107 These studies show that dietary LPC-DHA efficiently increases brain DHA content and impr

108 ction of AA, 2-AA-LPC, and 2-docosahexaenoyl-LPC that was over 10-fold greater than wild-type mitocho

109 Moreover, an early LPC effect was observed only for switched nouns, but not

110 is associated with the late parietal effect (LPC).

111 g that emotional stimuli can induce enhanced LPC.

112 15-hydroxyeicosatetraenoic acid (HETE) ether-LPC sn-1 esterification is markedly activated by thrombi

113 iency-corrected reprogramming rates of fetal LPCs were 275-fold higher, compared with unsorted fetal

114 ke, confirming the specificity of MFSD2A for LPCs having mono- and polyunsaturated fatty acyl chains.

115 hese findings indicate an essential role for LPCs in human brain development and function and provide

116 h was markedly enriched in EVs isolated from LPC-treated hepatocytes versus untreated cells.

117 Deletion of RELB and CYLD from LPCs protects mice from DDC-induced cholestatic liver fi

118 cholate is involved in initiating functional LPC biliary differentiation and the development of the D

119 Furthermore, LPC-mediated activation of type II NKT cells leads to an

120 to assess its functional role, we generated LPC organoids derived from patients with cirrhosis.

121 ficantly inhibited the production of 12-HETE-LPC and 12-HETE-LPE in activated platelets.

122 ccompanied by significant changes in 12-HETE-LPC in murine serum that were also markedly attenuated b

123 stream 12-LOX oxidation products, 12(S)-HETE-LPC and 12(S)-HETE-LPE, in calcium ionophore (A23187)-st

124 eak concentration, in the presence of a high LPC concentration, which is related to less degradation

125 However, LPC numbers also correlate with disease severity and hep

126 These findings identify LPC transport via Mfsd2a as an important pathway for DHA

127 in primary sensory neurons, and we identify LPC 18:1 as a previously unknown endogenous activator of

128 actively represents retrieved content or if LPC activity only scales with content reactivation elsew

129 Importantly, LPC 18:1 and LPC 16:0 can induce Ca(2+) transients in pr

130 cholate induced a time-dependent increase in LPC proliferation and expression of genes associated wit

131 As encoding enzymes and proteins involved in LPC degradation (lysophosphatidylcholine acyltransferase

132 oreover, recall-related activity patterns in LPC, but not VTC, differentiated between individual even

133 Longitudinal PET studies in LPC and EAE rat models demonstrate that [11C]MeDAS uptak

134 he IL-22 signaling pathway, was activated in LPCs isolated from DDC-fed IL-22TG mice.

135 nds where VDUP1 expression was maintained in LPCs, inhibiting both cell proliferation and lamina neur

136 n LSCs, including quiescent LSCs, but not in LPCs.

137 lpha/beta-dependent RIPK1 phosphorylation in LPCs inhibits compensatory proliferation of hepatocytes

138 ith combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed

139 reover, mice lacking both RIPK1 and TNFR1 in LPCs displayed normal tumor formation in response to DEN

140 is the key enzyme mediating the p25-induced LPC production and cPLA2 upregulation is critical in tri

141 Taurocholate induced LPCs to release MCP-1, MIP1alpha, and RANTES into condit

142 tes increased the induction of liver injury, LPC proliferation, and tumor necrosis factor-alpha produ

143 The aim of this study was to investigate LPC markers in AH and its correlation with disease sever

144 ortant, if not the dominant, source of known LPCs.

145 e and the other two players' evoked a larger LPC than the medium difference and the even condition.

146 almitoyl-, stearoyl-, oleoyl-, and linoleoyl-LPC levels after LCA exposure.

147 ent stem cells in fetal and postnatal liver (LPCs) can differentiate into both hepatocytes and cholan

148 containing L-alpha-lysophosphatidylcholine (LPC), as observed using atomic force microscopy.

149 ncreases in LPE and lysophosphatidylcholine (LPC) contents in leaves.

150 lglycerol (MAG) and lysophosphatidylcholine (LPC) hydrolytic activities, indicating the bifunctional

151 LPA and lysophosphatidylcholine (LPC) levels in the tumor microenvironment were reduced t

152 lysolipids LGL1 and lysophosphatidylcholine (LPC).

153 ormal adult mice as lysophosphatidylcholine (LPC) (40 mg DHA/kg) for 30 days increased DHA content of

154 ospholipids such as lysophosphatidylcholine (LPC) can stimulate the sulfatide-reactive type II NKT hy

155 eaction, as well as lysophosphatidylcholine (LPC), lipids shown to activate thermogenesis in brown ad

156 levated atherogenic lysophosphatidylcholine (LPC 18:1) and lysophosphatidic acids (LPAs) in the intes

157 ation in the brain, lysophosphatidylcholine (LPC)-induced focal demyelination in the spinal cord, and

158 ed sodium-dependent lysophosphatidylcholine (LPC) symporter expressed at the blood-brain barrier that

159 a sodium-dependent lysophosphatidylcholine (LPC) transporter (MFSD2A), expressed in the endothelium

160 he sodium-dependent lysophosphatidylcholine (LPC) transporter major facilitator superfamily domain co

161 showed that dietary lysophosphatidylcholine (LPC)-DHA significantly increases brain DHA, which result

162 addition of either lysophosphatidylcholine (LPC) or lysophosphatidic acid (LPA) to cells restored th

163 Finally, lysophosphatidylcholine (LPC) levels in the PFC were found to be correlated with

164 n produces LPA from lysophosphatidylcholine (LPC) via lysophospholipase D activity, but alternative e

165 dic acid (LPA) from lysophosphatidylcholine (LPC).

166 e D that hydrolyzes lysophosphatidylcholine (LPC) into lysophosphatidic acid (LPA), initiating signal

167 disease, including lysophosphatidylcholine (LPC).

168 emifusion inhibitor lysophosphatidylcholine (LPC), but not if a complementary-shaped lipid, oleic aci

169 e lysophospholipids lysophosphatidylcholine (LPC) 18:1 and LPC 16:0 were significantly increased 24 h

170 f lysophospholipids lysophosphatidylcholine (LPC) 18:1, LPC 16:0, and 9,10-EpOME in oxaliplatin-induc

171 uble lipid mediator lysophosphatidylcholine (LPC) is released by p25 overexpressing neurons to initia

172 r concentrations of lysophosphatidylcholine (LPC) led to an increase of the MscL/MscS threshold ratio

173 ribe our studies of lysophosphatidylcholine (LPC) presentation by human CD1d and its recognition by a

174 anced production of lysophosphatidylcholine (LPC) species by TSC2-deficient tumor cells.

175 s the conversion of lysophosphatidylcholine (LPC) to lysophosphatidic acid (LPA), a bioactive lipid a

176 r the hydrolysis of lysophosphatidylcholine (LPC) to the bioactive lysophosphatidic acid (LPA) and ch

177 ined the effects of lysophosphatidylcholine (LPC) upon microglia.

178 cids in the form of lysophosphatidylcholine (LPC).

179 y microinjection of lysophosphatidylcholine (LPC).

180 earoyl-, and oleoyl-lysophosphatidylcholine (LPC) and marked increases in tauro-beta-muricholate, tau

181 linating effects on lysophosphatidylcholine (LPC) induced demyelination in a three-dimensional brain

182 d with palmitate or lysophosphatidylcholine (LPC).

183 pc1, which produces lysophosphatidylcholine (LPC), and LPC can be converted to PC by the lysophosphol

184 enzymatic product, lysophosphatidylcholine (LPC), are involved in blood-retinal barrier (BRB) damage

185 of proinflammatory lysophosphatidylcholine (LPC), which was detectable in both HFD and MCD mice, was

186 h more radiolabeled lysophosphatidylcholine (LPC)-DHA enters the brain than NEFA-DHA, this is due to

187 in decreased serum lysophosphatidylcholine (LPC) and sphingomyelin levels due to elevated lysophosph

188 udy, we reveal that lysophosphatidylcholine (LPC), a molecule associated with neurodegeneration and d

189 hile treatment with lysophosphatidylcholine (LPC) enhanced the expression of iNOS, demonstrating a no

190 sion complexes with lysophosphatidylcholine (LPC), that decrease the susceptibility of amylose to amy

191 PG) or zwitterionic lysophosphatidylcholine (LPC) stimulate aggregation, LPG exerted a greater effect

192 of chemoprotective lysophosphatidylcholines (LPCs).

193 idylethanolamines, lysophosphatidylcholines (LPCs), sphingolipids, and cholesteryl esters all showed

194 Moreover, LPC markers correlated with liver expression and circula

195 Moreover, LPC-DHA treatment markedly improved the spatial learning

196 roliferation of cultured BMOL cells (a mouse LPC line).

197 drives the differentiation status of murine LPCs into the progenitor/cholangiocyte lineage while inh

198 human CD1d and its recognition by a native, LPC-specific iNKT TCR.

199 sociated liver tumors (Nemo(LPC-KO) and Nemo(LPC-KO)Cxcr6(eGfp/eGfp) mice).

200 epatocyte apoptosis and liver tumors in NEMO(LPC-KO) mice, revealing distinct kinase-dependent and sc

201 vented hepatocellular damage and HCC in NEMO(LPC-KO) mice.

202 l transfer experiments, and analyses of Nemo(LPC-KO) mice, we found that NKT and CD4 T cells promote

203 re senescent hepatocytes than livers of Nemo(LPC-KO) mice.

204 Livers of Nemo(LPC-KO)Cxcr6(eGfp/eGfp) mice had significantly more sene

205 p inflammation-associated liver tumors (Nemo(LPC-KO) and Nemo(LPC-KO)Cxcr6(eGfp/eGfp) mice).

206 amming efficiency of LPCs, compared with non-LPCs.

207 eta-catenin, and surface markers with normal LPCs.

208 LPA, but not LPC, also enhanced in vivo ascites formation (by approxi

209 LPA, but not LPC, stimulated ID8 cell migration and invasion with cel

210 ependent on the digestion time and amount of LPC.

211 ylate either sn position of ether analogs of LPC The data show that the activities of LPEAT1 and LPEA

212 ffects were particularly evident in areas of LPC (namely, angular gyrus) in which activity scaled wit

213 We investigated the capacity of LPC to differentiate into hepatocytes in vivo and contri

214 CDE models indicated that no contribution of LPC to hepatocytes was associated with LPC expression of

215 protein reporter mice, to follow the fate of LPC and biliary cells.

216 The generation of LPC by PMVECs required Prdx6-PLA2 We propose that Prdx6-

217 ulates NOX2 activation through generation of LPC for conversion to LPA; binding of LPA to LPAR1 signa

218 2 modulates NOX2 activation by generation of LPC that is converted to LPA by the lysophospholipase D

219 olyclonal, consisting of tens to hundreds of LPC clones.

220 ency in mice resulted in decreased import of LPC esterified to long chain fatty acids into activated

221 cyte-derived macrophages in the induction of LPC proliferation using clodronate liposome deletion of

222 rogenic genes, likely adaptations to loss of LPC transport.

223 beta(+) biliary duct cells are the origin of LPC.

224 roscopy demonstrated that in the presence of LPC as opposed to cholesterol, N-ethylmaleimide-sensitiv

225 Direct comparison of the uptake rate of LPC-DHA and NEFA-DHA demonstrates that uptake of NEFA-DH

226 croarray analysis showed an up-regulation of LPC markers in patients with AH.

227 To understand the role of LPC and LPCAT in acyl trafficking we produced and analyz

228 However, the origin and role of LPC in liver physiology and in hepatic injury remains a

229 However, the functional significance of LPC activation during memory retrieval remains a subject

230 ing to spread to cells distal to the site of LPC substrate binding by ATX.

231 haly syndrome linked to inadequate uptake of LPC lipids.

232 ferentiation toward hepatocyte-like cells of LPCs with high ALDH activity is also successfully applic

233 ificantly increased plasma concentrations of LPCs containing mono- and polyunsaturated fatty acyl cha

234 athways implicated in the differentiation of LPCs are still incompletely understood.

235 The increased reprogramming efficiency of LPCs, compared with differentiated liver cells, occurred

236 ed the increased reprogramming efficiency of LPCs, compared with non-LPCs.

237 High ALDH activity is a feature of LPCs that can be taken advantage of to isolate these cel

238 Mechanistically, import of LPCs was required to maintain T cell homeostatic turnove

239 Proliferation of LPCs in mice was induced by feeding a diet that containe

240 factor for hepatocytes, on proliferation of LPCs in patients with chronic hepatitis B virus (HBV) in

241 ings link inflammation with proliferation of LPCs in patients with HBV infection.

242 oduce IL-22, which promotes proliferation of LPCs via STAT3.

243 r-alpha, and the subsequent proliferation of LPCs.

244 e grade of inflammation and proliferation of LPCs.

245 g adenovirus, had increased proliferation of LPCs.

246 inflammation might promote proliferation of LPCs.

247 ers of IL-22TG mice reduced proliferation of LPCs.

248 More importantly, the increased ratio of LPCs to PCs of each irradiation group compared to contro

249 Significantly, biliary fate selection of LPCs was not observed in the absence of hepatocytes nor

250 CMCs was not correlated with bevacizumab or LPC treatment.

251 f experimental evidence establishing BECs or LPCs as the origin of ICCs, other liver cell types have

252 onfigurations of neighboring particle pairs (LPC-NPPs) to understand this emergent tetratic order and

253 Additionally, a peripheral LPC 18:1 injection was sufficient to induce mechanical h

254 higher amounts of lyso phosphatidylcholine (LPC) compared to SP2/0 and CHO cell lines.

255 phatidic acid, and lyso-phosphatidylcholine (LPC) have all been implicated in ER-to-chloroplast lipid

256 treal bevacizumab or laser photocoagulation (LPC) and untreated eyes.

257 and Firmicutes and Cyanobacteria with plasma LPC 18:1.

258 Ex vivo, ATX plus LPC or LPA itself induces the polarization of mouse naiv

259 ndent fatty acid release and polyunsaturated LPC production.

260 Human CD1d presenting LPC adopts an altered conformation from that of CD1d pre

261 rected hepatocyte differentiation of primary LPCs and pluripotent stem cells, findings of transdiffer

262 ed genomic instability in LSCs and primitive LPCs, which could be targeted to prevent the relapse and

263 n species (ROS) in CML-CP LSCs and primitive LPCs.

264 evolution were assessed: LPC proliferation, LPC biliary differentiation, and hepatic stellate cell (

265 DHA-deficient and had significantly reduced LPC/DHA transport in vivo Fluorescein angiography indica

266 /beta(LPC-KO) ) were intercrossed with RIPK1(LPC-KO) or RIPK3(-/-) mice to examine whether RIPK1 or R

267 an association between the changes in serum LPC and bile acids and proinflammatory cytokines.

268 is through TGF-beta signaling and that serum LPC is a biomarker for biliary injury.

269 A-DHA into the brain is 10-fold greater than LPC-DHA.

270 t diabetes-mediated BRB dysfunction and that LPC impacts on the retinal vascular endothelium to induc

271 hese findings provide striking evidence that LPC not only signals that memories have been successfull

272 d this emergent tetratic order and show that LPC-NPPs can be useful for predicting orientational orde

273 This study suggests that LPC proliferation may be an important feature of AH path

274 We demonstrate for the first time that LPC 18:1 contributes to the activation of the ion channe

275 The LPC component has higher influence on wafer shape change

276 The LPC has been shown to be generally sensitive to correct

277 The LPC maps indicate presence of a twist in the lattice pla

278 the HPC intervention compared with after the LPC intervention.

279 After epitaxial layer growth, the LPC variation across the wafer increases by a factor of

280 iNKT TCR requires a 7-A displacement of the LPC headgroup but stabilizes the CD1d-LPC complex in a c

281 n accompanied by decreased expression of the LPC receptor G2A, whereas MS patient samples show increa

282 Differences in the amplitude of the LPC were observed between correct and incorrect source d

283 so revealed differences, suggesting that the LPC is also sensitive to variations in the strength of s

284 tion in vivo These findings suggest that the LPC-mediated lipid signaling is involved in oxaliplatin-

285 Furthermore, alteration of the LPCs and Lpcat1/2/4 and Smpd3 expression was attenuated

286 ct cells and to assess their contribution to LPC expansion and hepatocyte generation.

287 d at the blood-brain barrier that transports LPCs containing DHA and other long-chain fatty acids.

288 tion to acyl-CoA, GPCAT efficiently utilizes LPC and lysophosphatidylethanolamine as acyl donors in t

289 ison showed distinct behaviors of LPG versus LPC monomers and micelles plausibly originating from the

290 nal thickening at the foveal center, whereas LPC is associated with earlier extrusion of the inner re

291 theories are divided with respect to whether LPC actively represents retrieved content or if LPC acti

292 on of LPC to hepatocytes was associated with LPC expression of genes related to telomere maintenance,

293 Slow catalysis with LPC reveals the potential for LPA signaling to spread to

294 d hydrolysis are slow and rate-limiting with LPC.

295 In contrast, mice with LPC-specific knockout of Ripk1 showed reduced diethylnit

296 cells following two liver injury models with LPC expansion, a diethoxycarbonyl-1,4-dihydro-collidin (

297 c factor increased in all brain regions with LPC-DHA, but not with free DHA.

298 Eyes treated with LPC had a lower probability of having all inner retinal

299 for and compare content reactivation within LPC and VTC.

300 ethyl-N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl))-LPC.