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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
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.

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