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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
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
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
24 cation of SMase leads to a redistribution of sphingomyelin and a reduction in forskolin- and VX-770-s
27 FO*), whereas another pool is sequestered by sphingomyelin and cannot be bound by PFO* unless the sph
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 (
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
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
42 resulted in increased cellular retention of sphingomyelin and significantly decreased incorporation
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
47 e abundant ceramides, which are converted to sphingomyelins and glucosylceramides/gangliosides by the
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.
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
67 sphatidylinositol (but not diacylglycerol or sphingomyelin) are significantly elevated in NECL4-defic
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
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
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
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
88 ith increased risk of T2D and serum glycine; sphingomyelin C16:1; acyl-alkyl-phosphatidylcholines C34
91 as changes in ceramide phosphoethanolamines, sphingomyelin, carnitines, tyrosine derivates and pantho
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
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
107 ride and phosphatidylethanolamine, and lower sphingomyelin concentrations in LCHF vs. HCLF milk.
109 n explicit lipid bilayers (DEPC, POPC, DMPC, sphingomyelin), confirming the observed dependence of th
111 vated enzyme activity in vitro and increased sphingomyelin content (mainly C22:0- and C24:0-sphingomy
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
117 t lipid classes such as phosphatidylcholine, sphingomyelin, diglycerides, and triglycerides were dete
120 referential localization of cholesterol- and sphingomyelin-enriched microdomains in the collar band o
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
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
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
137 ltering the concentration of cholesterol and sphingomyelin in ternary mixtures does not alter 5-HT1A
140 tivity is known to depend on the presence of sphingomyelin in the target membrane and is enhanced by
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
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)
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
158 itional simulation of EqtII with an N-acetyl sphingomyelin micelle, for which high-resolution NMR dat
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
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
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
178 phages that showed that transcription of the sphingomyelin phosphodiesterase acid-like 3A (SMPDL3A) g
180 proteinuria possibly associated with loss of sphingomyelin phosphodiesterase acid-like 3b (SMPDL-3b).
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
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
195 nge experiments revealed that 70-80% of cell sphingomyelin resided in the plasma membrane outer leafl
198 M fractions were enriched in cholesterol and sphingomyelin, similar to that found with plasma membran
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
209 explore how the nature of the acyl chains of sphingomyelin (SM) influence its lateral distribution in
211 e-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glio
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
216 Palmitate (a) induced the accumulation of sphingomyelin (SM) precursors such as sphinganine, dihyd
218 ography-tandem mass spectrometry to identify sphingomyelin (SM) species coupled with immunoblot analy
220 f oxysterol-binding protein (OSBP) regulates sphingomyelin (SM) synthesis, as well as post-Golgi chol
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
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
236 e (IPC) synthase, and TbSLS4, a bifunctional sphingomyelin (SM)/ethanolamine phosphorylceramide (EPC)
238 which binds cholesterol in membranes; (2) a sphingomyelin(SM)-sequestered pool that binds 125I-PFO*
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
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
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.
260 MTP deficiency had no effect on ceramide and sphingomyelin synthesis but reduced secretion from prima
262 e mimicked by treatment with cholesterol and sphingomyelin synthesis inhibitors (mevastatin and myrio
265 BP were both required for 25OH activation of sphingomyelin synthesis, suggesting that 25OH must be ex
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
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
281 lamydial infection but reduced the amount of sphingomyelin trafficked to the inclusion in infected ce
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
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
292 Of the measured plasma sphingolipids, five sphingomyelins were associated with emphysema; four trih
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
299 ed an association of phosphatidylcholine and sphingomyelin with inflammation and myo-inositol with ce
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