ライフサイエンスコーパス: sphingomyelin

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

2 Erythrocyte membranes contain up to 27% sphingomyelin.

3 ole in the regulation of plasma ceramide and sphingomyelin.

4 a lipid mediator formed by the metabolism of sphingomyelin.

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

6 ich catalyzes the formation of ceramide from sphingomyelin.

7 A peak at 703.3 Da was assigned as a sphingomyelin.

8 h generates the main mammalian sphingolipid, sphingomyelin.

9 ance nanopores in lipid membranes containing sphingomyelin.

10 t Nanodiscs containing lipid-raft associated sphingomyelin.

11 ubstitutions at this site allow transport of sphingomyelin.

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

13 amines, nucleotide derivatives, phenols, and sphingomyelins.

14 d normal levels of acylcarnithins but not of sphingomyelins.

15 4, lysophosphatidylcholine 17:0, and hydroxy-sphingomyelin 14:1) were associated with red meat consum

16 ructural changes of phosphatidylcholine plus sphingomyelin (2.4:1) model lipid membranes.

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

18 ound in HM and MM; HM and CaM were richer in sphingomyelin (78.3 and 117.5mug/ml) and plasmalogens (2

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

20 Sphingomyelin, a major lipid localized exclusively on th

21 RNA) knockdown of VAMP4 inhibited chlamydial sphingomyelin acquisition, correlating with a log decrea

22 ts further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER st

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

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

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

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

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

28 Both sphingomyelin and ceramide are important components of l

29 hanolamine lipids, decreased C-16 containing sphingomyelin and ceramide lipid levels, and a dramatic

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

31 ncristine sulfate liposome injection (VSLI), sphingomyelin and cholesterol nanoparticle vincristine (

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

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

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

35 These toxins cleave the substrates sphingomyelin and lysophosphatidylcholine in mammalian t

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

37 reatment with dsRNA resulted in increases in sphingomyelin and morphologic changes including increase

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

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

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

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

42 resulted in increased cellular retention of sphingomyelin and significantly decreased incorporation

43 Cholesterol, in alliance with sphingomyelin and specialized proteins, enforces a more

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

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

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

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

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

49 choline-containing phospholipids, including sphingomyelins and phosphatidylcholines.

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

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

52 of chain-branching in glycerophospholipids, sphingomyelins and triacylglycerols and thus can be used

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

54 revented by cotreatment with cholesterol and sphingomyelin, and can be mimicked by treatment with cho

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

56 ylcholine, dioleoylphosphatidylethanolamine, sphingomyelin, and cholesterol (molar ratio of 35:30:15:

57 mitoplasts, whereas other ceramide species, sphingomyelin, and diacylglycerol were without effect.

58 species including ceramide, dihydroceramide, sphingomyelin, and hexosylceramide.

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

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

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

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

63 phatidylethanolamines, phosphatidylcholines, sphingomyelins, and lysophosphatidylcholines were unchan

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

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

66 Subphenotyping suggests that sphingomyelins are strongly associated with emphysema an

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

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

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

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

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

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

73 tidylinositol, phosphatidylethanolamine, and sphingomyelin between phospholipid vesicles.

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

75 We propose a model in which cholesterol and sphingomyelin binding to the TCRbeta chain causes TCR di

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

77 SMS is the last enzyme for sphingomyelin biosynthesis, and SMS2 is one of its isofo

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

79 icles thus critically relies on a functional sphingomyelin biosynthetic pathway, required to drive in

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

81 Sphingomyelin breakdown as a result of sphingomyelinase

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

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

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

85 everse reaction, production of ceramide from sphingomyelin, but none of the Ala substitutions of the

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

87 Here, we report that depletion of sphingomyelin by inhibitors or sphingomyelinase caused p

88 ith increased risk of T2D and serum glycine; sphingomyelin C16:1; acyl-alkyl-phosphatidylcholines C34

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

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

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

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

93 res of palmitoyl-oleoyl-phosphatidylcholine, sphingomyelin, ceramide, and 10 mol % cholesterol.

94 Lipids atypical for plastids (sphingomyelins, ceramides, and cholesterol) were detecte

95 ylcholine, dioleoylphosphatidylethanolamine, sphingomyelin, cholesterol, and dioleoylphosphatidylseri

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

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

98 /1,2-dioleoyl-3-sn-phosphatidylethanolamine/ Sphingomyelin/Cholesterol (35:30:15:20) membranes, their

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

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

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

102 es (1,2-dioleoyl-sn-glycero-3-phosphocholine/sphingomyelin/cholesterol) into liquid-disordered (l(d))

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

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

105 ajor epidermal lipids, such as ceramides and sphingomyelins, compared with wild-type mice at differen

106 These changes were also reflected in sphingomyelin composition.

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

108 Serum sphingomyelin concentrations were inversely correlated (

109 n explicit lipid bilayers (DEPC, POPC, DMPC, sphingomyelin), confirming the observed dependence of th

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

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

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

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

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

115 Our control data showing cholesterol and sphingomyelin dependence as well as independence of acti

116 Furthermore, specific sphingomyelins, diacylglycerols, and ether phospholipids

117 t lipid classes such as phosphatidylcholine, sphingomyelin, diglycerides, and triglycerides were dete

118 in macrophages indicating that Mtb utilizes sphingomyelin during infection.

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

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

121 g of dioleoylphosphatidylcholine (DOPC), egg sphingomyelin (eSM), and cholesterol (Chol).

122 S4 was shown previously to be a bifunctional sphingomyelin/ethanolamine phosphorylceramide synthase,

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

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

125 phosphatidylcholine, phosphatidylserine, and sphingomyelin from the cytoplasmic to the exocytoplasmic

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

127 nvolved a redox-regulated translocation of a sphingomyelin hydrolase (neutral sphingomyelinase-2) to

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

129 Ceramide, the product of sphingomyelin hydrolysis, is detected in newly formed pa

130 membrane environment conferred by depleting sphingomyelin impairs PS flip and promotes cholesterol e

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

132 type tissues the amount of C16:0 containing sphingomyelin in kidney is approximately 35%, whereas we

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

134 d by microscopy in giant vesicles containing sphingomyelin in place of diC(18:0) PC.

135 cerophosphocholine, phosphatidylcholine, and sphingomyelin in several tissues.

136 Depletion of sphingomyelin in stably transfected HEK293 cells express

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

138 Ceramide produced from sphingomyelin in the plasma membrane is purported to aff

139 to changes in the levels of cholesterol and sphingomyelin in the plasma membrane.

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

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

142 the distribution of bioactive ceramides and sphingomyelin in tissues.

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

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

145 cell-free liposome studies that showed that sphingomyelin increased the rate of spontaneous PS flipp

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

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

148 ASMase converts sphingomyelin into the signaling lipid, ceramide.

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

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

151 Sphingomyelin is the main sphingolipid in Trypanosoma br

152 A treatment also resulted in decreased serum sphingomyelin levels and increased hepatic ceramide leve

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

154 ased serum lysophosphatidylcholine (LPC) and sphingomyelin levels due to elevated lysophosphatidylcho

155 defects demonstrated decreased ceramide and sphingomyelin levels in the cell plasma membranes, as we

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

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

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

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

160 Membranes made of Chol/ESM (cholesterol/egg sphingomyelin) mixtures were investigated using saturati

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

162 of other endomembranes, bundle ceramide and sphingomyelin nearly exclusively contain short-chain, sa

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

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

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

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

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

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

169 phatidylcholines, phosphatidylethanolamines, sphingomyelins, phosphatidylserines, phosphatidylglycero

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

171 sphatidylcholine acyltransferase (LPCAT) and sphingomyelin phosphodiesterase (SMPD) expression.

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

173 on functionally characterizing 2 candidates, sphingomyelin phosphodiesterase 3 (SMPD3) and neurofilam

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

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

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

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

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

179 This screen identified the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g

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

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

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

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

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

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

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

187 upts this transport in response to excessive sphingomyelin production.

188 Docking of sphingomyelin provides a model that allows insight into

189 Thermal behavior of N-palmitoyl sphingomyelin (PSM) and N-palmitoyl ceramide (PCer) mixt

190 model membrane system composed of palmitoyl sphingomyelin (PSM), cholesterol, and an unsaturated lip

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

192 or-alpha-induced increase in the ceramide-to-sphingomyelin ratio in the caveolae, and inhibits cytoki

193 te (S1P), whereas the levels of ceramide and sphingomyelin remain unchanged.

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

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

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

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

198 M fractions were enriched in cholesterol and sphingomyelin, similar to that found with plasma membran

199 Sphingomyelin (SM) and cholesterol (Chol)-enriched micro

200 hatidylcholine (PDPC-d(31)) in mixtures with sphingomyelin (SM) and cholesterol (chol).

201 deficiency of NSMase2 resulted in storage of sphingomyelin (SM) and cholesterol with a 50% reduction

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

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

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

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

206 artially reversed lipotoxic reductions in ER sphingomyelin (SM) content and aggregation of ER lipid r

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

208 hatidylcholine (PC) in the inner leaflet and sphingomyelin (SM) in the outer leaflet.

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

210 Sphingomyelin (SM) is a vital component of mammalian mem

211 e-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glio

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

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

214 r phospholipid components of the outer leaf, sphingomyelin (SM) nor phosphatidylcholine (PC), evinces

215 Asymmetric LUVs in which sphingomyelin (SM) or SM + 1-palmitoyl-2-oleoyl-phosphat

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

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

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

219 Sphingomyelin (SM) species exhibited neither an increase

220 f oxysterol-binding protein (OSBP) regulates sphingomyelin (SM) synthesis, as well as post-Golgi chol

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

222 t ciliogenic ceramide is derived from apical sphingomyelin (SM) that is endocytosed and then converte

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

224 sphingomyelinase (ASMase) converts the lipid sphingomyelin (SM) to phosphocholine and ceramide and ha

225 f phosphatidylcholine (PC) and 13 species of sphingomyelin (SM) were identified from the molecular io

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

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

228 , PC, PG, with 40 mol % cholesterol; and 3), sphingomyelin (SM), PG, with 40 mol % cholesterol.

229 hesis is the conversion of ceramide (Cer) to sphingomyelin (SM), which is catalyzed by sphingomyelin

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

231 We observed that lysenin-positive sphingomyelin (SM)-rich rafts are identified histochemic

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

233 nzyme of the de novo biosynthetic pathway of sphingomyelin (SM).

234 lum to the Golgi complex for conversion into sphingomyelin (SM).

235 tive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM).

236 e (IPC) synthase, and TbSLS4, a bifunctional sphingomyelin (SM)/ethanolamine phosphorylceramide (EPC)

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

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

239 Sphingomyelins (SMs) and ceramides are known to interact

240 Sphingomyelins (SMs) are plasma membrane lipids that und

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

242 ans double bond for the unique properties of sphingomyelins (SMs), one of the main lipid components i

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

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

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

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

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

248 mains are formed in model membranes at lower sphingomyelin (Sph) content than needed for the large-sc

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

250 cyclodextrin) and the enzymatic breakdown of sphingomyelin (sphingomyelinase), results in significant

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

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

253 to sphingomyelin (SM), which is catalyzed by sphingomyelin synthase (SMS).

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

255 T) subunit 2 (Sptlc2) gene knockout mice and sphingomyelin synthase 2 (Sms2) gene knockout mice.

256 We also tested the atypical sphingomyelin synthase isoform, SMSr, for its role in th

257 Cells genetically deficient in sphingomyelin synthase-1 (SGMS1) or blocked in their syn

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

259 Sphingomyelin synthases (SMS) and sphingomyelin phosphod

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

261 ool of which is generated as a by-product of sphingomyelin synthesis from ceramide.

262 e mimicked by treatment with cholesterol and sphingomyelin synthesis inhibitors (mevastatin and myrio

263 Fyn silencing did not alter sphingomyelin synthesis or trafficking in the absence of

264 sicle trafficking to the plasma membrane and sphingomyelin synthesis, respectively.

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

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

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

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

269 We propose that phosphatidylcholine and sphingomyelin (the major external phospholipids of healt

270 ific enrichment of lysobisphosphatidic acid, sphingomyelin, the ganglioside GM3, and cholesterol este

271 Sphingomyelin, the most abundant nuclear sphingolipid, p

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

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

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

275 uggesting that conversion of plasma membrane sphingomyelin to ceramide by this lysosomal enzyme promo

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

277 of cell fate and signaling via hydrolysis of sphingomyelin to form ceramide.

278 myelinase (ASM) is an enzyme that hydrolyzes sphingomyelin to produce ceramide.

279 host proteins involved in the trafficking of sphingomyelin to the chlamydial inclusion.

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

281 lamydial infection but reduced the amount of sphingomyelin trafficked to the inclusion in infected ce

282 The reduced sphingomyelin trafficking caused by downregulation of th

283 Notably, VAMP4 knockdown inhibits sphingomyelin trafficking only to inclusions in which it

284 ins whose deficiency significantly decreased sphingomyelin trafficking to the inclusion and 16 protei

285 ins whose deficiency significantly increased sphingomyelin trafficking to the inclusion were identifi

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

287 Host sphingomyelin was associated with C. trachomatis isolate

288 Mechanistically, sphingomyelin was connected to PS translocation in cell-

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

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

291 Both cholesterol and sphingomyelin were required for the formation of TCR dim

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

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

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

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

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

297 However, phosphatidylcholine and sphingomyelin which are the primary PL constituents of n

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

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

300 decreased saturated phosphatidylcholine and sphingomyelin within the T cells.