ライフサイエンスコーパス: sphingomyelin

1 h generates the main mammalian sphingolipid, sphingomyelin.

2 ance nanopores in lipid membranes containing sphingomyelin.

3 t Nanodiscs containing lipid-raft associated sphingomyelin.

4 ubstitutions at this site allow transport of sphingomyelin.

5 te the transport of a novel lipid substrate, sphingomyelin.

6 ells and enriched in long fatty acid (C16:0) sphingomyelin.

7 Erythrocyte membranes contain up to 27% sphingomyelin.

8 ole in the regulation of plasma ceramide and sphingomyelin.

9 a lipid mediator formed by the metabolism of sphingomyelin.

10 cs simulations on N-palmitoyl and N-stearoyl sphingomyelin.

11 ttle effect on cholesterol in complexes with sphingomyelin.

12 can also bind non-activating lipids, such as sphingomyelin.

13 ingomyelinase (ASM), an enzyme that degrades sphingomyelin.

14 ds, diacylglycerides, triacylglycerides, and sphingomyelins.

15 idylcholines, phosphatidylethanolamines, and sphingomyelins.

16 d normal levels of acylcarnithins but not of sphingomyelins.

17 MTARC1 was associated with higher levels of sphingomyelins.

18 4, lysophosphatidylcholine 17:0, and hydroxy-sphingomyelin 14:1) were associated with red meat consum

19 gredients constitute concentrated sources of sphingomyelin (3.4-21mg/g dry matter) and contained low

20 es potent sphingomyelinase activity cleaving sphingomyelin, a major lipid in eukaryotic cells, into c

21 ariety of glycerolipids and the sphingolipid sphingomyelin across membranes.

22 h sphingomyelin and cholesterol, reveal that sphingomyelin adopts two distinct conformations in membr

23 itoyl lyso-phosphatidylethanolamine and lyso-sphingomyelin) also facilitated the lateral segregation

24 Here, we report that sphingomyelin, an abundant lipid of the luminal leaflet

25 ngomyelinase (SMase), an enzyme that cleaves sphingomyelin, an alpha toxin receptor.

26 elopmental Cell, Sundberg et al. reveal that sphingomyelin and a proteoglycan mediate lipoprotein lip

27 cation of SMase leads to a redistribution of sphingomyelin and a reduction in forskolin- and VX-770-s

28 lux, luminal acidification, and cleared both sphingomyelin and Abeta from lysosomes.

29 riability in entry requirements for cellular sphingomyelin and acid sphingomyelinase activity.IMPORTA

30 calized to lysosomes that were engorged with sphingomyelin and calcium.

31 FO*), whereas another pool is sequestered by sphingomyelin and cannot be bound by PFO* unless the sph

32 mvastatin reduced the relative proportion of sphingomyelin and ceramide to phosphatidylcholine (q=0.0

33 Sphingomyelin and cholesterol are essential lipids that

34 nds to membranes only when they contain both sphingomyelin and cholesterol, reveal that sphingomyelin

35 When assaying liposomes containing sphingomyelin and cholesterol, we observed an overall gr

36 This gap is addressed by showing that sphingomyelin and cholesterol-rich (SCOR) lipid mixtures

37 properties among C16:0 sphingomyelin, C24:0 sphingomyelin and cholesterol.

38 ayer of unsaturated PL/N-palmitoyl-D-erythro-sphingomyelin and cholesterol.

39 We found higher levels of sphingomyelin and lower levels of cardiolipin, among oth

40 reference for choline, the headgroup of both sphingomyelin and lysophosphatidylcholine, versus ethano

41 Lastly, this is the first report of sphingomyelin and lysosomal sphingomyelinase playing a r

42 anolamine (PE) levels, while hippocampal PC, sphingomyelin and PE levels were elevated.

43 cells harbored several molecular species of sphingomyelin and phosphatidylcholine as its ligands.

44 These results indicate that sphingomyelin and phosphatidylcholine lipids can act as

45 it is found that two of these phospholipids, sphingomyelin and phosphatidylcholine, have the highest

46 oach to map the dynamics of Atto646N-labeled sphingomyelin and phosphatidylethanolamine in the plasma

47 Inhibition of ASM elevates cellular sphingomyelin and reduces cellular ceramide levels.

48 -II increased ceramide species but decreased sphingomyelin and sphingosine-1-phosphate concentrations

49 cellular lipids, including the sphingolipids sphingomyelin and sphingosine.

50 VP* formation, whereas other lipids, such as sphingomyelin and sulfatide, either did not affect ISVP*

51 trast to ASMase, SMPDL3A is inactive against sphingomyelin and, surprisingly, can instead hydrolyze n

52 Thus, sphingomyelin and/or cholesterol binding to the transmem

53 ically relevant substrates are thought to be sphingomyelin and/or lysophosphatidylcholine.

54 ar also reduced triglycerides, diglycerides, sphingomyelins and ceramides.

55 e abundant ceramides, which are converted to sphingomyelins and glucosylceramides/gangliosides by the

56 ctive variant in MTARC1 to the metabolism of sphingomyelins and identify distinct molecular patterns

57 es in plasma levels of phosphatidylcholines, sphingomyelins and others in just 6 days.

58 cid, and associated changes to metabolism of sphingomyelins and phosphatidylcholines.

59 lysophosphocholines, 72 phosphocholines, 10 sphingomyelins and sum of hexoses) and 5 lifestyle risk

60 ( approximately 37 mol %), a mixture of SM (sphingomyelin) and DOPC (dioleoylphosphatidylcholine) in

61 hosphatidylethanolamine (DOPE), bovine brain sphingomyelin, and cholesterol (35:30:15:20 molar ratio)

62 ary mixtures of dioleoylphosphatidylcholine, sphingomyelin, and cholesterol were used to form phase-s

63 ations between phosphatidylethanolamines and sphingomyelin, and glycine-serine and sphingomyelin, obs

64 determined that anionic lipids, cholesterol, sphingomyelin, and membrane fluidity play critical roles

65 domains are tightly packed with cholesterol, sphingomyelin, and saturated fatty acids, whereas disord

66 cells myriocin decreased cellular ceramide, sphingomyelin, and sphingosine-1-phosphate content.

67 have a reduction in membrane cholesterol and sphingomyelin, and upon TCR triggering they exhibit alte

68 acylcarnitines, 81 glycerophospholipids, 14 sphingomyelins, and ferritin were determined in serum sa

69 phatidylethanolamines, phosphatidylcholines, sphingomyelins, and lysophosphatidylcholines were unchan

70 etabolites and decreased levels of steroids, sphingomyelins, and phosphatidylcholines distinguished p

71 ylcholines, phosphatidylethanolamines (PEs), sphingomyelins, and triacylglycerols (TAGs) were associa

72 Subphenotyping suggests that sphingomyelins are strongly associated with emphysema an

73 sphatidylinositol (but not diacylglycerol or sphingomyelin) are significantly elevated in NECL4-defic

74 ne lipids, such as transferrin receptors and sphingomyelin, are delivered to the lysosomes.

75 Sphingomyelinases generate ceramide from sphingomyelin as a second messenger in intracellular sig

76 n Mtb rv0888 deletion mutant did not grow on sphingomyelin as a sole carbon source anymore and replic

77 membrane protein that enables Mtb to utilize sphingomyelin as a source of several essential nutrients

78 her in-depth multi-omics analysis identified sphingomyelins as key secreted factors, and their role w

79 onset of GADA-first was preceded by reduced sphingomyelins at infancy.

80 Perturbing the plasma membrane cholesterol/sphingomyelin balance abrogated vesicle formation.

81 Perturbing the cholesterol/sphingomyelin balance was shown to induce narrow tubular

82 ous radius of curvature for pure N-palmitoyl sphingomyelin bilayers is estimated to be 43-100 A, depe

83 nzene pendants to various locations near the sphingomyelin binding pocket of FraC with the aim of rem

84 Remarkably, lysenin (a sphingomyelin-binding protein) also bound preferentially

85 exiting the ER to activate SPT and increase sphingomyelin biosynthesis, which may buffer excess cell

86 his analytical method, added cholesterol and sphingomyelin, both neutral and not themselves displaced

87 Sphingomyelin breakdown as a result of sphingomyelinase

88 somes through myelin debris accumulation and sphingomyelin build-up induces lysosomal damage and cath

89 se successfully reduced cell surface-exposed sphingomyelin but did not significantly inhibit BoHV-1 e

90 had significantly lower plasma ceramide and sphingomyelin but normal hexosylceramide, lactosylcerami

91 hingomyelin content (mainly C22:0- and C24:0-sphingomyelin) but lower hexosylceramide (Hex-Cer) level

92 y is facilitated by phosphatidylglycerol and sphingomyelin, but dominantly inhibited by cholesterol t

93 ncreased in the presence of erythrocytes and sphingomyelin by 5- and 100-fold, respectively.

94 -pathways were enriched by all methods, and 'sphingomyelins' by all but Wilcoxon, indicating these pa

95 e helix appears to selectively bind a single sphingomyelin C18:0 molecule.

96 Serial first- (sphingomyelin C18:1 and urea) and third-trimester (hexos

97 mparative analysis of properties among C16:0 sphingomyelin, C24:0 sphingomyelin and cholesterol.

98 8:1/20:0, d18:1/20:1, d18:1/22:1), saturated sphingomyelins (C34:0, C36:0, C38:0, C40:0), unsaturated

99 ns (C34:0, C36:0, C38:0, C40:0), unsaturated sphingomyelins (C34:1, C36:1, C42:3), hydroxyl-sphingomy

100 hingomyelins (C34:1, C36:1, C42:3), hydroxyl-sphingomyelins (C34:1, C38:3), and a hexosylceramide (d1

101 as changes in ceramide phosphoethanolamines, sphingomyelin, carnitines, tyrosine derivates and pantho

102 The mechanism by which sphingomyelin catalysis inhibits CFTR is not known but e

103 Our CCS database comprises sphingomyelin, cerebroside, ceramide, phosphatidylethano

104 mized lipid formulation was comprised of egg-sphingomyelin, cholesterol, and polyethylene glycol dist

105 iosides associate laterally with each other, sphingomyelin, cholesterol, and select proteins in lipid

106 Vs of ternary lipid mixtures composed of egg sphingomyelin, cholesterol, and the negatively charged l

107 two formulations of CPD100: one composed of sphingomyelin/cholesterol (55/45; mol/mol) (CPD100Li) an

108 In cells, levels of sphingomyelin/cholesterol complexes are held constant ov

109 esterol, properties that are consistent with sphingomyelin/cholesterol complexes.

110 line/dioleoylphosphatidylethanolamine (DOPE)/sphingomyelin/cholesterol in a molar ratio of 35:30:15:2

111 When liposomes poor in sphingomyelin/cholesterol or mimicking the lipid composi

112 ol/mol) (CPD100Li) and the other composed of sphingomyelin/cholesterol/PEG (55/40/5; mol/mol) (CPD100

113 tios between PC:phosphatidylethanolamine and sphingomyelin:cholesterol, as well as by modified phosph

114 had higher dihydroceramides, ceramides, and sphingomyelins compared with children with nonallergic a

115 These changes were also reflected in sphingomyelin composition.

116 ride and phosphatidylethanolamine, and lower sphingomyelin concentrations in LCHF vs. HCLF milk.

117 Serum sphingomyelin concentrations were inversely correlated (

118 toxin, which self-inserts open channels into sphingomyelin containing membranes and is known to be vo

119 anemone that oligomerizes and forms pores in sphingomyelin-containing membranes.

120 vated enzyme activity in vitro and increased sphingomyelin content (mainly C22:0- and C24:0-sphingomy

121 to promote virion infectivity by decreasing sphingomyelin content in the virion.

122 re, and could be caused by a decrease of the sphingomyelin content of the diseased lipid mixture.

123 oxycholesterol did not affect total cellular sphingomyelin content or its lysosomal distribution.

124 Accordingly, the cholesterol and sphingomyelin contents of sciatic nerves were greatly re

125 tidylethanolamine (PE), cardiolipin (CL) and sphingomyelin contents were higher in the Montanera pigs

126 to hypothesise that the enrichment of C16:0 sphingomyelin could determine enhanced dynamic propertie

127 SMPD3 controls homeostasis of the sphingomyelin cycle in the Golgi compartment, essential

128 Among these lipids, sphingomyelin-d18:1/14:0 and mono-hexosylceramide-d18:1/

129 Collectively, our analysis suggests that sphingomyelin-d18:1/14:0, mono-hexosylceramide-d18:1/20:

130 us pseudorabies virus (PRV) was inhibited by sphingomyelin-depletion of cells.

131 To monitor subcellular sphingomyelin distribution, we generated a live sphingom

132 in macrophages indicating that Mtb utilizes sphingomyelin during infection.

133 hanolamine inhibit and phosphatidic acid and sphingomyelin enhance SPCA1a activity.

134 referential localization of cholesterol- and sphingomyelin-enriched microdomains in the collar band o

135 des, lactosylceramides, or other unsaturated sphingomyelins (even if having an SFA base) were not ass

136 eoylphosphatidylcholine (POPC)) and egg-yolk sphingomyelin (EYSM) lipids, and allowed us to extract s

137 tidylinositol, phosphatidylethanolamine, and sphingomyelin, fatty acids 12:0 and 14:0 were high, as w

138 The preferential localization of sphingomyelin, ganglioside GM1 and cholesterol in the mo

139 In contrast, decreased sphingomyelines, hexosylceramide and lactosylceramide in

140 , but only de novo synthesis inhibition, not sphingomyelin hydrolysis, improved glucose tolerance and

141 lost saturated very long fatty acid (C24:0) sphingomyelin in cancer cells and enriched in long fatty

142 hatidylcholine, phosphatidylethanolamine and sphingomyelin in lipid extracts in the VV group compared

143 ically, they colocalize with cholesterol and sphingomyelin in ordered membrane domains.

144 ltering the concentration of cholesterol and sphingomyelin in ternary mixtures does not alter 5-HT1A

145 tivity is known to depend on the presence of sphingomyelin in the target membrane and is enhanced by

146 ectivity of JFH-1 by decreasing the level of sphingomyelin in the virion.

147 the distribution of bioactive ceramides and sphingomyelin in tissues.

148 mpositions involving phosphatidylcholine and sphingomyelin in which the acyl chain lengths of these l

149 ver, ToF-SIMS revealed a steady depletion of sphingomyelin in white matter regions during 28d Li-trea

150 We speculate that secreted sphingomyelins in the mammary gland of mammals with a na

151 The percentage of sphingomyelin increased following pasteurization, with n

152 reased membrane order induced by sterols and sphingomyelin increases receptor-catalyzed oligonucleoti

153 version of the lipid cell membrane component sphingomyelin into ceramide.

154 ASMase converts sphingomyelin into the signaling lipid, ceramide.

155 nsin II; two lipids, phosphatidylcholine and sphingomyelin; Irganox 1010 (a detergent); insulin; and

156 yelin and cannot be bound by PFO* unless the sphingomyelin is destroyed with sphingomyelinase (SMase)

157 In its second conformation, sphingomyelin is free from cholesterol and does not bind

158 rough two distinct successive stages: first, sphingomyelin is gradually translocated into the cytosol

159 that MTP might regulate plasma ceramide and sphingomyelin levels by transferring these lipids to B-l

160 Sphingomyelin levels were found to be high in adjacent n

161 line, phosphatidylethanolamine, ceramide and sphingomyelin lipid groups, for example, in males, 17.04

162 hatidylethanolamine, phosphatidylserine, and sphingomyelin lipids did not induce an increase of wild

163 idylcholines, acylcarnitine, amino acids and sphingomyelins; Lyso.PC.a.C18.0, PC.ae.C34.2, C3.DC..C4.

164 Some species of glycerophosphoinositol, sphingomyelin, lysophosphatidylcholine and cholesterol s

165 findings suggest that a cluster of saturated sphingomyelins may be associated with elevated risk of d

166 This study identifies sphingomyelin metabolism as an indirect regulator of K-R

167 patients, suggesting metabolic re-wiring of sphingomyelin metabolism in MacTel patients.

168 itional simulation of EqtII with an N-acetyl sphingomyelin micelle, for which high-resolution NMR dat

169 The miscibility of milk sphingomyelin (milk-SM) and cholesterol was investigated

170 uld be related to the respective cholesterol/sphingomyelin molar ratio in the three milk species.

171 es and sphingomyelin, and glycine-serine and sphingomyelin, observed in controls, were reduced in Mac

172 amounts of bioactive ceramides in a ratio to sphingomyelin of 1:5mol% in buttermilk and 1:10mol% in b

173 Exposure of sphingomyelin on BCVs may therefore act as an early dang

174 interaction can exist either with palmitoyl sphingomyelin or with dipalmitoyl phosphatidylcholine an

175 idylcholine, distearoyl phosphatidylcholine, sphingomyelin, or galactosylceramide, used as substrates

176 fluorescent cholesterol analog, with oleoyl sphingomyelin (OSM) was significantly stronger than its

177 terol is driven toward the inner leaf by the sphingomyelin phosphatidylcholine mixture.

178 at describes the outer leaf as consisting of sphingomyelin, phosphatidylcholine, and cholesterol and

179 nt ceramides in mixed bilayers together with sphingomyelin, phosphatidylcholine, and cholesterol.

180 s containing phosphatidic acid together with sphingomyelins, phosphatidylethanolamine, and cholestero

181 Unsaturated phosphatidylcholines, sphingomyelins, phosphatidylethanolamines, glucosylceram

182 Sphingomyelin synthases (SMS) and sphingomyelin phosphodiesterase (SMase) enzymes may play

183 SMPD1 (sphingomyelin phosphodiesterase 1) was activated by vent

184 n by VSMCs, most likely by the activation of sphingomyelin phosphodiesterase 3 (SMPD3) and cytoskelet

185 Sphingomyelin phosphodiesterase 3 (SMPD3), a lipid-metab

186 ed extracellular calcium was found to induce sphingomyelin phosphodiesterase 3 expression and the sec

187 m VSMCs in vitro, and chemical inhibition of sphingomyelin phosphodiesterase 3 prevented VSMC calcifi

188 and CD81, and their release was regulated by sphingomyelin phosphodiesterase 3.

189 phages that showed that transcription of the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g

190 proteinuria possibly associated with loss of sphingomyelin phosphodiesterase acid-like 3b (SMPDL-3b).

191 The lipid-modulating enzyme sphingomyelin phosphodiesterase acid-like 3B (SMPDL3b) i

192 sphingolipids and the lipid-modifying enzyme sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) i

193 Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b) i

194 Sphingomyelin phosphodiesterase, acid-like 3A (SMPDL3A)

195 increased by lipids, including sphingosine, sphingomyelin, platelet-activating factor, and lysophosp

196 ese molecules can modulate both ceramide and sphingomyelin pools in cells and inhibit cell migration.

197 investigation of the respective ceramide and sphingomyelin populations in L3.6pl cells revealed that

198 extracellularly within seconds to hydrolyze sphingomyelin preferentially enriched in outer plasma me

199 gomyelins, suggesting that they may act upon sphingomyelin processing enzymes.

200 Specifically, we show that sphingomyelin production at the TGN triggers a signallin

201 upts this transport in response to excessive sphingomyelin production.

202 Docking of sphingomyelin provides a model that allows insight into

203 R study on membranes consisting of palmitoyl sphingomyelin (PSM) and palmitoyl ceramide (PCer).

204 presented for ternary mixtures of palmitoyl sphingomyelin (PSM), cholesterol, and either palmitoyl o

205 ingomyelin distribution, we generated a live sphingomyelin reporter from Lysenin, a sphingomyelin-spe

206 De novo synthesis of the sphingolipid sphingomyelin requires non-vesicular transport of cerami

207 nge experiments revealed that 70-80% of cell sphingomyelin resided in the plasma membrane outer leafl

208 a toxin that upon binding to the surface of sphingomyelin-rich cells undergoes a structural metamorp

209 We conclude that sphingomyelin-rich marginal cells act as a sink to scave

210 cargo sorting into secretory vesicles with a sphingomyelin-rich membrane; the integral membrane prote

211 While sphingomyelin-rich, high-order lipid regions near certai

212 tions were attenuated and only the saturated-sphingomyelin score remained associated with risk of dia

213 Therefore, MTP is involved in ceramide and sphingomyelin secretion but not in their synthesis.

214 fer targeting of SDC1 and bound LPL into the sphingomyelin secretion pathway.

215 modules, and 2 modules containing saturated sphingomyelins showed the strongest associations with in

216 eir role was confirmed via inhibition of the sphingomyelin signaling pathway.

217 Under some conditions, a sphingomyelin (SM) and cholesterol-rich ordered domain i

218 increase in ceramide (Cer) and a decrease in sphingomyelin (SM) and dihydrosphingomyelin (dhSM) level

219 ton X-100 of binary mixtures composed of egg sphingomyelin (SM) and either ceramide, diacylglycerol,

220 c proteins that bind to membranes containing sphingomyelin (SM) and oligomerize to form pores.

221 line and cholesterol plus different types of sphingomyelin (SM) are prone to produce bilayer regions

222 ylserine (PS), phosphatidylcholine (PC), and sphingomyelin (SM) cations with dicarboxylate anions are

223 xamined the influence of hydrogen bonding on sphingomyelin (SM) colipid interactions in fluid uni- an

224 hanolamine (PE), phosphatidic acid (PA), and sphingomyelin (SM) in a safe manner by removing any need

225 ents in all cell lines with lower amounts of sphingomyelin (SM) in SP2/0 compared to CHO and HEK, whi

226 nt studies in cell model systems showed that sphingomyelin (SM) in the outer leaflet of the plasma me

227 explore how the nature of the acyl chains of sphingomyelin (SM) influence its lateral distribution in

228 Sphingomyelin (SM) is the most abundant sphingolipid in

229 ses (SMases), resulting in elevated cellular sphingomyelin (SM) levels and altered SM distribution.

230 cyl species and phosphatidylcholine (PC) and sphingomyelin (SM) lipids.

231 f cisterna morphology led us to propose that sphingomyelin (SM) metabolism at the trans-Golgi membran

232 Palmitate (a) induced the accumulation of sphingomyelin (SM) precursors such as sphinganine, dihyd

233 different circulating Cer species, and their sphingomyelin (SM) precursors, with heart failure have r

234 Absorption of dietary sphingomyelin (SM) requires its initial degradation into

235 ography-tandem mass spectrometry to identify sphingomyelin (SM) species coupled with immunoblot analy

236 Sphingomyelin (SM) species exhibited neither an increase

237 In particular, sphingomyelin (SM) species were significantly up-regulat

238 Do lipids such as sphingomyelin (SM) that are known to assemble into speci

239 essed in intestinal mucosa, which hydrolyses sphingomyelin (SM) to ceramide and inactivates platelet

240 s mixtures containing a high-Tm lipid (brain sphingomyelin (SM)) or dipalmitoyl phosphatidylcholine (

241 gi is the principal site of the synthesis of sphingomyelin (SM), an abundant sphingolipid that is tra

242 lesterol and saturated phospholipids such as sphingomyelin (SM), may form.

243 elevation in phosphatidylethanolamine (PE), sphingomyelin (SM), phosphatidylcholine (PC) and their m

244 mbranes and has a favorable interaction with sphingomyelin (SM), together forming domains in the liqu

245 he strong attraction between cholesterol and sphingomyelin (SM), which is predominantly in that leaf.

246 stion in cell biology and biophysics whether sphingomyelin (SM)- and cholesterol (Chol)- driven nanod

247 The second is a sphingomyelin (SM)-sequestered pool inaccessible to PFO

248 cyl-chain lengths and their interaction with sphingomyelin (SM).

249 We have examined how saturated sphingomyelin (SM; palmitoyl and stearoyl SM (PSM and SS

250 Phosphatidylcholines (PC) and sphingomyelins (SM) were the most abundant phospholipids

251 which binds cholesterol in membranes; (2) a sphingomyelin(SM)-sequestered pool that binds 125I-PFO*

252 were observed in di- and triacylglycerides, sphingomyelins (SMs), lysophosphatidylcholines (LysoPCs)

253 d profile analysis demonstrated increases in sphingomyelin species and sphingosine concurrently with

254 ography tandem mass spectrometry to identify sphingomyelin species coupled with immunoblotting analys

255 Multiple tumor specific ceramide and sphingomyelin species were detected and confirmed by on-

256 teins and have been shown to bind a specific sphingomyelin species.

257 live sphingomyelin reporter from Lysenin, a sphingomyelin-specific toxin from the earthworm Eisenia

258 that CARDS TX binds phosphatidylcholine and sphingomyelin specifically over other membrane lipids, a

259 ed due to aggregate formation, revealed that sphingomyelin specificity might occur via hydrogen bondi

260 Therefore 10,12-pentacosadyinoic acid (PCDA)/Sphingomyelin(SPH)/Cholesterol(CHO)/Lysine system was te

261 We demonstrate that sphingomyelin stabilizes caveolae to the cell surface, w

262 ased levels of specific low molecular weight sphingomyelins, suggesting that they may act upon sphing

263 The screening on mammalian sphingomyelin synthase (SMS) and glucosylceramide syntha

264 y investigates the consequences of elevating sphingomyelin synthase 1 (SMS1) activity, which generate

265 We find that expression of sphingomyelin synthase 5 (SMS-5) in the marginal cells i

266 differences in their metabolic conversion by sphingomyelin synthase and glucosylceramide synthase.

267 date genes, including sms-1, which encodes a sphingomyelin synthase.

268 Sphingomyelin synthases (SMS) and sphingomyelin phosphod

269 MTP deficiency had no effect on ceramide and sphingomyelin synthesis but reduced secretion from prima

270 BP were both required for 25OH activation of sphingomyelin synthesis, suggesting that 25OH must be ex

271 ment of ceramide transfer protein (CERT) for sphingomyelin synthesis.

272 ansferase (SPT), the rate-limiting enzyme in sphingomyelin synthesis.

273 stallizing wactive we identify a presumptive sphingomyelin-synthesis pathway that is necessary for cr

274 a had lower dihydroceramides, ceramides, and sphingomyelins than did controls.

275 p7 and NS5B, as well as an interaction with sphingomyelin that regulates virion infectivity.

276 The interactions of the ceramides with sphingomyelin, their lateral segregation into ceramide-r

277 Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and phosphocholine, essential

278 pithelium, the conversion of apical membrane sphingomyelin to ceramide by exogenous bacterial sphingo

279 elinase (SMase) catalyzes the degradation of sphingomyelin to ceramide.

280 1, the acid sphingomyelinase that hydrolyzes sphingomyelin to ceramide.

281 linase 2 (nSMase2) catalyzes the cleavage of sphingomyelin to phosphorylcholine and ceramide, an esse

282 vity is sufficient to target transferrin and sphingomyelin to the lysosomes.

283 erol, 2) increased cancer cell catabolism of sphingomyelins to ceramide derivatives and 3) altered ce

284 t included lower serum phosphatidylcholines, sphingomyelins, tryptophan, ornithine, and citrulline, a

285 Host sphingomyelin was associated with C. trachomatis isolate

286 lcholines and phospholipid ethers, and lower sphingomyelins was protective for mAb+ in the nested cas

287 lthough a potential substrate for SMPDL3B is sphingomyelin, we identify other possible substrates suc

288 ans isomers completely, as was the case with sphingomyelins, we relied upon the aforementioned diagno

289 ed specifically in caveolae, cholesterol and sphingomyelin were actively sequestered, whereas glycosp

290 Of the measured plasma sphingolipids, five sphingomyelins were associated with emphysema; four trih

291 Most previous force fields for sphingomyelins were developed before the availability of

292 ly induced, while several acylcarnithins and sphingomyelins were found significantly downregulated up

293 ccumulate in tissues, specific ceramides and sphingomyelins were identified by on-tissue isolation an

294 family lipids, such as lysophospholipids or sphingomyelin, were found significantly (p<0.05) differe

295 , exoplasmic leaf is rich in cholesterol and sphingomyelin, whereas the inner, cytoplasmic leaf is ri

296 Due to its favorable interaction with sphingomyelin, which is almost entirely in the outer lea

297 ng cholesterol accessibility by depletion of sphingomyelin, which sequesters cholesterol in complexes

298 ed an association of phosphatidylcholine and sphingomyelin with inflammation and myo-inositol with ce

299 1.24, 4.65; P-trend = 0.003) and a score of sphingomyelins with fully saturated sphingoid-fatty acid

300 decreased saturated phosphatidylcholine and sphingomyelin within the T cells.