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1 both sLeX and 3-sulfated galactosylceramide (sulfatide).
2 e II NKT cells recognize the self-glycolipid sulfatide.
3 id-transfer protein effectively present lyso-sulfatide.
4 s that recognize lipid components such as O4 sulfatide.
5 pids, and variations of the self-glycolipid, sulfatide.
6 rine, phosphatidylinositol, cholesterol, and sulfatide.
7 rebroside (GalC) and its sulfated derivative sulfatide.
8  galactolipids galactocerebroside (GalC) and sulfatide.
9 there was an exceptionally strong binding to sulfatide.
10 rebroside (GalC) and its sulfated derivative sulfatide.
11 containing hydroxylated fatty acids and with sulfatide.
12  alter selectin binding to sLex, heparin, or sulfatide.
13 N-terminal domain binds liposomes containing sulfatide.
14 eramide (GalCer) and its sulfated derivative sulfatide.
15 th micromolar affinities similar to that for sulfatide.
16  was found to contain 17 gangliosides and 13 sulfatides.
17  to the laminin coiled-coil dystroglycan and sulfatides.
18 of myelin 2-hydroxy galactosylceramides and -sulfatides.
19  by treatment of the substrate with SGGLs or sulfatides.
20 s for TSP1, heparan sulfate proteoglycan and sulfatides.
21  responsible for the lysosomal hydrolysis of sulfatides.
22 ng, including phospholipids, cholesterol and sulfatides.
23 eficient (ASA knockout) mice that accumulate sulfatides.
24 tides and 10 to 1,000 nM for C16:0 and C24:0 sulfatides.
25           We used chamber slides coated with sulfatide (3-O-sulfogalactosylceramide) to provide a bas
26 lethanolamines, 2 phosphatidylinositols), 10 sulfatides (5 hydroxylated species and 5 nonhydroxylated
27 -[14C]arachidonoyl-phosphati dylethanolamine:sulfatide (70:0.2:30) were incubated with the supernatan
28 s lipid binding activity with preference for sulfatide, a glycosphingolipid present in the outer leaf
29                  Neutrophils stimulated with sulfatide, a ligand for the L-selectin receptor, or the
30 ein for arylsulfatase A in the hydrolysis of sulfatide, a lipid component of myelin.
31 We now show that SC expression of galactosyl-sulfatide, a Lm-binding glycolipid, precedes that of Lms
32                                We identified sulfatide, a major constituent of CNS myelin, as a novel
33 egulatory mechanism following recognition of sulfatide, a self-glycolipid ligand for a subset of CD1d
34                                              Sulfatide accumulated, but galactosylceramide remained a
35  loss of Sap B function leads to progressive sulfatide accumulation in satellite cells surrounding th
36                                 We show that sulfatide accumulation significantly impacts the formati
37  that these inclusion bodies corresponded to sulfatide accumulation.
38                    We therefore suggest that sulfatides act as counterions for interstitial ammonium
39 ids (in particular galactocerebroside and/or sulfatide) act as sensors and/or transmitters of environ
40 e platelet surface, and platelets expressing sulfatides adhere to P-selectin.
41 NS-resident microglia, are inactivated after sulfatide administration, and mice deficient in type I N
42 vine submaxillary mucins, and the glycolipid sulfatide, all of which present multivalent sialylated a
43  Strikingly, we found that the glycolipid Ag sulfatide also localized almost exclusively to early end
44 such that it is able to adhere to heparin or sulfatide and can reduce P-selectin adherence to these l
45                     These data indicate that sulfatide and complex b-series gangliosides on the glial
46 o assess the functional interactions between sulfatide and gangliosides, CST (-/-) and GalNAc-T (-/-)
47 in are important in 987P fimbrial binding to sulfatide and glycoprotein receptors, suggesting differe
48                Thus, autoimmune responses to sulfatide and other lipids are present in individuals wi
49 omal storage of the acidic glycosphingolipid sulfatide and progressive demyelination.
50 r range of 5 to 1,000 nM for C18:0 and C24:1 sulfatides and 10 to 1,000 nM for C16:0 and C24:0 sulfat
51                                 Moreover, 71 sulfatides and 59 polar phospholipids (phosphatidylserin
52 normal nerve function.SIGNIFICANCE STATEMENT Sulfatides and complex gangliosides are membrane glycoli
53 Here, we show vital interdependent roles for sulfatides and complex gangliosides because double (but
54                  These findings suggest that sulfatides and complex gangliosides on opposing axo-glia
55          In negative ion mode, MALDI favored sulfatides and free fatty acids, whereas NAPA spectra we
56                                              Sulfatides and gangliosides are raft-associated glycolip
57 te that two classes of sulfated glycolipids, sulfatides and HNK-1-reactive sulfoglucuronylglycolipids
58  type II NKT cells recognizes myelin-derived sulfatides and is selectively enriched in the CNS tissue
59          The lectin domain of brevican binds sulfatides and SGGLs in a calcium-dependent manner as ex
60 Intact, full-length brevican also binds both sulfatides and SGGLs.
61 er beta2-glycoprotein I forms a complex with sulfatides and thereby becomes a target for anti-phospho
62 d by phosphatidylcholine, sphingomyelin, and sulfatides and were not substantially stimulated by cere
63 roteoglycan, 3-sulfated galactosyl ceramide (sulfatide), and heparin.
64 directed against galactocerebroside sulfate (sulfatide); and RMAb, which is directed against galactoc
65 a1 contains major binding sites for heparin, sulfatide, and alpha-dystroglycan and plays a critical r
66 amide, glucosylceramide, galactosylceramide, sulfatide, and globotriaosylceramide are abnormally incr
67 inding to collagen IV, to bind to galactosyl sulfatide, and to selectively convert alpha-short arm de
68 nd CHO cells expressing P-selectin adhere to sulfatides, and anti-P-selectin antibodies inhibit this
69 ones corresponding to phosphatidylinositols, sulfatides, and gangliosides were recorded in negative i
70 hosphoethanolamines, glycerophospho-serines, sulfatides, and gangliosides.
71 th diverse targets such as heparan sulfates, sulfatides, and integrins on cell surfaces.
72 hermore, both anti-P-selectin antibodies and sulfatide antagonist MCSP significantly reverse platelet
73 e data presented here indicate that GalC and sulfatide are essential in proper CNS node and paranode
74                                              Sulfatides are expressed on the platelet surface, and pl
75 blasts become competent for BM assembly when sulfatides are intercalated into their cell surfaces.
76                                              Sulfatides are most highly modulated by wild-type p53 tr
77 de carrier(s) in human CSF demonstrated that sulfatides are specifically associated with apoE-contain
78                                              Sulfatides are sulfated glycosphingolipids expressed on
79                                              Sulfatides are sulfated glycosphingolipids present on th
80 c phospholipids, as commonly known, but also sulfatides are targets for most anti-phospholipid antibo
81                Sulfated galactosylceramides (sulfatides) are glycosphingolipids associated with chole
82 ously that an antibody to galactocerebroside/sulfatide arrested terminal differentiation, suggesting
83 can powerfully inhibit axon growth, identify sulfatide as a novel myelin-associated axon growth inhib
84                     Thus, we have identified sulfatide as a self-lipid recognized by human iNKT cells
85               Here, we show a novel role for sulfatides as a major ligand for P-selectin in platelet
86 ost of the false positives identified by the sulfatide assay.
87 mouse CD1d in complex with cis-tetracosenoyl sulfatide at 1.9 A resolution reveals that the longer ci
88 bound CD1d is inefficient in presenting lyso-sulfatide at neutral pH, it is efficiently presented at
89                            The nonhydrolyzed sulfatide-Azure A is recovered and measured at a wavelen
90 total sulfatide used in the enzyme reaction (sulfatide-Azure A present in a parallel assay performed
91 rfaces decreased the immunoreactivity toward sulfatide-beta2-glycoprotein I complex by >50% in 12 of
92                                    Selective sulfatide binding may indicate possible function for GSD
93 ed by site-directed mutagenesis to study its sulfatide binding properties.
94 residues within SBP that are responsible for sulfatide binding.
95                                         Dab2 sulfatide-binding motif contains two helices when embedd
96 e of a Dab2-derived peptide encompassing the sulfatide-binding motifs has been determined in dodecylp
97 inding peptide (SBP), contains two potential sulfatide-binding motifs represented by two consecutive
98 surface by binding to sulfatides through two sulfatide-binding motifs, modulating the extent of plate
99 region within Dab2, which we refer to as the sulfatide-binding peptide (SBP), contains two potential
100 d-binding in other proteins, suggesting that sulfatide-binding proteins share common binding mechanis
101                  Both sulfatide micelles and sulfatide-binding recombinant malaria circumsporozoite p
102 son to other sulfatides or alphaGalCer, lyso-sulfatide binds with lower affinity to CD1d.
103 he role of MmpL8-mediated lipid transport in sulfatide biogenesis, we insertionally inactivated the m
104  SL-1 are coupled and that the final step in sulfatide biosynthesis may be the extra-cellular esterif
105  the integrin alpha(IIb)beta(3) receptor and sulfatides, blocking their association to fibrinogen and
106 nct mode of recognition of a self-glycolipid sulfatide bound to CD1d by a type II NKT TCR.
107 et of anti-phospholipid antibodies, bound to sulfatide-bound beta2-glycoprotein I and previous absorp
108 antibodies from 4 of 5 patients reacted with sulfatide-bound beta2-glycoprotein I.
109 s a single species of sulfatide, namely lyso-sulfatide but not other sulfatides containing additional
110 CGT-deficient mice do not synthesize GalC or sulfatide but surprisingly form myelin containing glucoc
111  Beta2-glycoprotein I binds to surface-bound sulfatides but not to other glycolipids, such as ceramid
112       In addition, sulphogalactosylceramide (sulfatide) but not heparin can induce HPC mobilization.
113 JL/J mice with a synthetic cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses on
114                                              Sulfatide, but not galactocerebroside or ceramide, stron
115 bited the binding of laminin to bovine brain sulfatide, but not to its cell surface receptors on MCF-
116 branes immobilized with phosphoinositides or sulfatide, but not with cardiolipin.
117                         Since recognition of sulfatide by CD1d-restricted T cells has now been shown
118 ibly communicating with the sulfate group of sulfatide by hydrogen bonding and/or salt bridge formati
119 binding self-glycolipid ligands such as lyso-sulfatide can be presented via the secretory and endosom
120 er a single immunodominant form of synthetic sulfatide can treat ongoing chronic and relapsing EAE in
121                     Examination of potential sulfatide carrier(s) in human CSF demonstrated that sulf
122                                          The sulfatide/CD1d-tetramer(+) cells isolated from naive mic
123                            Mice deficient in sulfatide (cerebroside sulfotransferase knock-out, CST (
124 in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain li
125                                         At a sulfatide coating density of 1 microg/well, beta2-glycop
126  II NKT cell TCRs, therefore, recognize CD1d-sulfatide complexes by a distinct recognition mechanism
127  sulfatide in a manner that was dependent on sulfatide concentration and incubation temperature and i
128                              The increase in sulfatide concentration by a 14-mer prosaptide, TX14(A),
129      Herein prosaposin was found to increase sulfatide concentrations in primary and transformed Schw
130 posins, only saposin C was found to increase sulfatide concentrations in these cell types.
131                                              Sulfatides constitute a major component of myelin glycol
132  major myelin lipids galactosylceramides and sulfatides contain 2-hydroxy fatty acids.
133 lfatide, namely lyso-sulfatide but not other sulfatides containing additional acyl chains.
134                 Reduced levels of binding to sulfatide-containing liposomes correlated with reduced f
135  mutant (K117A) did not interact at all with sulfatide-containing liposomes.
136                             In contrast, the sulfatide content in brain tissues from human apoE4-expr
137                         TX14(A) enhanced the sulfatide content of primary Schwann cells by 2.5-fold,
138 phatidylethanolamine, phosphatidic acid, and sulfatide, critical for synaptic functions.
139                                        Renal sulfatide-deficient mice had lower urinary pH accompanie
140                                     Blocking sulfatide degradation from the saposin B deficiency dimi
141                               In addition to sulfatide-dependent loss of NF155, CST (-/-) x GalNAc-T
142              We found profound inhibition of sulfatide-dependent T cell proliferation which was parti
143                                              Sulfatide derived from the myelin stimulates a distinct
144  Assembly is characterized by coalescence of sulfatide, DG, and c-Src into a Lm-associated complex; b
145  abrogate 987P binding to the lipid receptor sulfatide did not affect the interaction with the glycop
146                          Mice unable to make sulfatide did not regenerate RGC axons more robustly aft
147 metachromatic leukodystrophy, who accumulate sulfatides due to a deficiency in arylsulfatase-A, direc
148 tail of CD1b to lysosomes, failed to present sulfatide efficiently.
149 reas other lipids, such as sphingomyelin and sulfatide, either did not affect ISVP* formation or prev
150                However, mycoplasmas bound to sulfatide exhibited no gliding motility, regardless of r
151 here, the histone H1 molecules stabilize the sulfatide-fimbriae interaction by simultaneously binding
152 onance shows that the affinity of human CD1d-sulfatide for the iNKT cell receptor is relatively low c
153 ce lacking the ability to synthesize GalC or sulfatide form dysfunctional and unstable myelin.
154 is obtained by subtracting the nonhydrolyzed sulfatide from the total sulfatide used in the enzyme re
155 by dextran sulfate 500K, dextran sulfate 5K, sulfatides, fucoidan, and heparin but not by chondroitin
156 ed by decreased brain levels of cholesterol, sulfatide, galactosylceramide, and triglyceride.
157 ed sphingolipid analogs of glucosylceramide, sulfatide, ganglioside GM1, ceramide 1-phosphate, sphing
158  matrix for imaging of acidic lipids such as sulfatides, gangliosides, and phosphatidylinositols in t
159 by 3'SL was least sensitive to inhibition by sulfatide, gastric mucin, and other sulfated oligosaccha
160 R42, is responsible for interaction with the sulfatide headgroup, whereas the C-terminal polybasic re
161                    Here, we demonstrate that sulfatides, highly charged anionic glycosphingolipids, a
162 H confirmed the novel role of this enzyme in sulfatide hydrolysis.
163  M. pneumoniae bound to surfaces coated with sulfatide in a manner that was dependent on sulfatide co
164  bind to sialylated receptors but adhered to sulfatide in a temperature-dependent manner.
165 eature of neuroinflammatory disease and that sulfatide in APCs may contribute to the endogenous pathw
166 lted in decreased sulfate incorporation into sulfatide in cultures of differentiating OL.
167                       Over 50% of GalCer and sulfatide in myelin is hydroxylated by the integral memb
168  NK T cell hybridomas is unable to recognize sulfatide in the presence of CD1d+ antigen-presenting ce
169 cell reactivity toward these GSLs and to the sulfatides in a fashion comparable with alpha-GalCer.
170                                              Sulfatides in brain lipid extract were also easily detec
171 esponsible for the catabolism and control of sulfatides in humans.
172 es a first step in understanding the role of sulfatides in regulating PDGFRalpha levels in OLs and it
173       This study points to a seminal role of sulfatides in renal ammonium handling, urinary acidifica
174 ts deficiency results in the accumulation of sulfatides in the cells of the central and peripheral ne
175 nse, suggesting an immunomodulatory role for sulfatides in the pathogenesis of tuberculosis.
176 ein I also depends on the coating density of sulfatides in the well.
177 icantly able to inhibit bacterial binding to sulfatide, indicating that in addition to glycoproteins,
178 elet mixture, reduces the number and size of sulfatide-induced aggregates.
179 PD-L pathway failed to prevent bacterial- or sulfatide-induced iNKT cell anergy, suggesting additiona
180  growth inhibitor, and provide evidence that sulfatide inhibition contributes to axon regenerative fa
181                                              Sulfatides interact with several cell adhesion molecules
182 oposed to play an essential role in the FasG-sulfatide interaction, possibly communicating with the s
183                      These results show that sulfatide interactions with P-selectin are important in
184                                          The sulfatide interactions with P-selectin stabilize platele
185 stricted type II NKT cell subset reactive to sulfatide involved in the regulation of autoimmunity and
186 o than was wild-type myelin, indicating that sulfatide is a major component of the inhibitory activit
187                         Presentation of lyso-sulfatide is inhibited in the presence of primaquine, co
188                               The hydrolyzed sulfatide is monitored upon inclusion of the colorimetri
189               Thus, ARSA activity toward the sulfatide is obtained by subtracting the nonhydrolyzed s
190                            Cis-tetracosenoyl sulfatide is one of the immunodominant species in myelin
191 by neuron- or glial-specific rescue, whereas sulfatide is principally expressed and functional in gli
192                              We propose that sulfatide is recognized only by human iNKT cells because
193 g of polar lipids including gangliosides and sulfatides is a necessary step in understanding the dive
194 substrate, galactosyl-3-sulfate ceramide (or sulfatide), is performed using neat sulfatide without ch
195  caused an increase in brain cholesterol and sulfatide levels in four major brain structures (hippoca
196 sterol and establish that it does not affect sulfatide levels in the brain, these levels did increase
197 g high density lipoproteins, suggesting that sulfatide levels in the central nervous system (CNS) are
198    Excess hydroxy and non-hydroxy fatty acid sulfatide levels were present in brain and kidney.
199                       Galactocerebroside and sulfatide, major galactosphingolipid components of oligo
200 urons and oligodendrocytes expressing the O4 sulfatide marker.
201                                          The sulfatide mass in hippocampus and cortex of apoE knockou
202 e that interactions of these antibodies with sulfatides may contribute to some of the clinical sympto
203 an serve as a second-tier test following the sulfatide measurement in DBS for newborn screening of ML
204                                              Sulfatide-mediated activation of type II NKT cells reduc
205 cells as well as after their inactivation by sulfatide-mediated activation of type II NKT cells.
206 ecause CD1 molecules are nonpolymorphic, the sulfatide-mediated immune-regulatory pathway can be targ
207               Protection from hepatic IRI by sulfatide-mediated inactivation of type I NKT cells was
208                    The mechanism involved in sulfatide-mediated inhibition may share features with ot
209                                         Both sulfatide micelles and sulfatide-binding recombinant mal
210  specifically recognizes a single species of sulfatide, namely lyso-sulfatide but not other sulfatide
211 i-galactolipid antibodies, showing that anti-sulfatide O4 but not anti-galactocerebroside O1 blocks t
212 he 3-hydroxyl group in the sphingoid base of sulfatides offered some protection from oxidation for th
213                 In this study, the effect of sulfatides on mouse T cell function and differentiation
214                     The inhibitory effect of sulfatides on T cell function was CD1d-independent and w
215 sed sulfated content of galactosylceramides (sulfatides) on the regulation of PDGFRalpha in multipote
216 glucopyranosylceramide (beta-GlcCer) but not sulfatide or phospholipids in a CD1d-dependent manner, w
217 not involved in P-selectin binding to either sulfatide or sLeX.
218                       In comparison to other sulfatides or alphaGalCer, lyso-sulfatide binds with low
219 uire membrane microdomains containing either sulfatides or complex gangliosides to localize and funct
220 erse lipids such as lysophosphatidylcholine, sulfatide, or mannosyl-phosophomycoketide, but not lipop
221 f MmpL8, which transports a precursor of the sulfatides, or MmpL11, which transports an unknown subst
222 receptor-activating peptide, suggesting that sulfatide-P-selectin interactions are necessary for the
223         These results indicate that GalC and sulfatide play important roles in myelin function and st
224                              Cholesterol and sulfatides play many important roles in learning and mem
225                    Immunization of mice with sulfatide plus myelin peptide resulted in a more severe
226          These structure and binding data on sulfatide presentation by CD1d have important implicatio
227 iNKT cells directly recognize myelin-derived sulfatide presented by CD1d.
228 ion reactive to a myelin-derived glycolipid, sulfatide, presented by CD1d.
229 ition of type I NKT cells by retinoids or by sulfatide prevents ALD.
230             Moreover, treatment of mice with sulfatide prevents antigen-induced experimental autoimmu
231 n of sulfatide-reactive type II NKT cells by sulfatide prevents induction of EAE.
232 elitis a model for human multiple sclerosis, sulfatide-reactive T cells but not invariant NK T cells
233 kine responses, we showed that activation of sulfatide-reactive type II NKT cells and plasmacytoid DC
234             We have shown that activation of sulfatide-reactive type II NKT cells by sulfatide preven
235          Collectively, the TCR repertoire of sulfatide-reactive type II NKT cells exhibits features o
236         We have shown that the activation of sulfatide-reactive type II NKT cells leads to a signific
237 IRI: type I NKT cells promote injury whereas sulfatide-reactive type II NKT cells protect against inj
238 ophosphatidylcholine (LPC) can stimulate the sulfatide-reactive type II NKT hybridoma Hy19.3 in a CD1
239 eviously determined A'-roof positioning of a sulfatide-reactive type II NKT TCR.
240 ate fimbrial binding to a glycoprotein and a sulfatide receptor on intestinal brush borders of piglet
241 ognized by human iNKT cells and propose that sulfatide recognition by innate T cells may be an import
242 y-determining region (CDR) loops, as well as sulfatide recognition separately encoded by nongermline
243  CD patient showed decreased cerebroside and sulfatide relative to normal white matter.
244 factors, IgG anti-GQ1b:GM4, GQ1b:PS and GQ1b:Sulfatide remained associated with faster recovery.
245     The Dab2 SBP residues that interact with sulfatides resemble those described for sphingolipid-bin
246 pe II NKT cells with antibody or the agonist sulfatide, respectively.
247 ctosylceramide and galactosylsphingosine and sulfatide, respectively.
248 malization of the ratio of long versus short sulfatides, restored PDGFRalpha levels, corrected its lo
249  TCR in complex with CD1d and the self-lipid sulfatide, revealing the unusual recognition of CD1d by
250 rain lipid metabolism (e.g., accumulation of sulfatides) seen in APOE-deficient mice, indicating func
251 al structure of human CD1a in complex with a sulfatide self antigen at a resolution of 2.15 A.
252  method to measure developmentally regulated sulfatide species (C16:0, C18:0, C24:1, and C24:0) in ce
253 ption of an analytical method to study these sulfatide species in raft and non-raft membranes and has
254                    Although it is known that sulfatide species show heterogeneity in their fatty acid
255                                     All four sulfatide species were more abundant in raft membranes t
256                                              Sulfatide-specific antibodies were also detected in SJL/
257 disease course of EAE, and administration of sulfatide-specific antibody exacerbated EAE.
258 ntly presented sulfatide to CD1a-restricted, sulfatide-specific T cells.
259 sis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebros
260 was, however, a marked effect of apoE on the sulfatide (ST) content in both the brain and CSF.
261 e recently noted a profound decline in brain sulfatides (ST) in subjects who died with incipient deme
262 rest, ganglioside GM2, asialo-GM2 (GA2), and sulfatides (ST).
263 lycerol (PG), phosphatidylinositol (PI), and sulfatides (ST).
264                                              Sulfatide stimulation in vitro led to prominent suppress
265                        Alcian blue positive (sulfatide) storage cells were found in the brain, spinal
266 y mimics that of the alkyl chain in the CD1a-sulfatide structure.
267 d blood spots (DBS) using deuterated natural sulfatide substrate.
268  95% failed to inhibit mycoplasma binding to sulfatide, suggesting that P1 does not mediate binding t
269 eramide, and the sulfated glycosphingolipids sulfatide, sulf-lactosylceramide, and sulf-globopentaosy
270 -3-sulfate-3-sulfohydrolase), which converts sulfatide (sulfogalactocerebroside) to galactocerebrosid
271                                 We disrupted sulfatide synthesis by a genetic approach along the enti
272 tivate ERKs, which is essential for enhanced sulfatide synthesis in Schwann cells.
273                          The PACAP effect on sulfatide synthesis was fully reproduced in a cerebellar
274 lated from human cerebrospinal fluid carries sulfatide that can be captured by APCs and presented by
275 ickling may expose normally cryptic membrane sulfatides that could mediate this adhesive interaction.
276                        With the exception of sulfatides, the invasion-inhibitory effect was not media
277  the platelet membrane surface by binding to sulfatides through two sulfatide-binding motifs, modulat
278 stigated presentation of the self-glycolipid sulfatide to a type II NKT cell that specifically recogn
279 ld-type CD1a molecules efficiently presented sulfatide to CD1a-restricted, sulfatide-specific T cells
280 se prevention correlates with the ability of sulfatide to suppress both interferon-gamma and interleu
281 it is not important for presentation of lyso-sulfatide to type II NKT cells.
282  possible function for GSDMB in the cellular sulfatide transport.
283                 Moreover, tolerized DCs from sulfatide-treated animals can adoptively transfer protec
284            After deacylation of bovine brain sulfatide under mild alkaline conditions and reacylation
285 g the nonhydrolyzed sulfatide from the total sulfatide used in the enzyme reaction (sulfatide-Azure A
286 e Sphingomonas glycosphingolipids (GSLs) and sulfatide variants were shown to activate human NKT cell
287  ceramide-1-phosphate, glucosylceramide, and sulfatide, via the C1q domain in an oligomerization-depe
288                              Myelin in which sulfatide was lacking or blocked using specific antibodi
289  binding to heparin, alpha-dystroglycan, and sulfatides was dependent upon both shared and unique con
290  that CD1d presenting self-lipids, including sulfatide, was widely recognized by gut Vdelta1+ gammade
291 lin-associated lipids galactocerebroside and sulfatide were modestly reduced in Igf1(-/-) brains.
292                                              Sulfatides were highly concentrated in the fetus liver,
293 ically selective images for cerebrosides and sulfatides were successfully obtained.
294 sitols, phosphatidylinositol-phosphates, and sulfatides) were scrutinized on rat brain tissue section
295 pports adhesion of cells expressing SGGLs or sulfatides, which was inhibited by monoclonal antibodies
296   Consistent with colocalization of CD1a and sulfatide, wild-type CD1a molecules efficiently presente
297 mologous series of ceramide monohexoside and sulfatide with hydroxylated fatty acyl chains ranging fr
298             First, FasG attaches strongly to sulfatide with hydroxylated fatty acyl chains.
299 en embedded in micelles, reversibly binds to sulfatides with moderate affinity, lies parallel to the
300 mide (or sulfatide), is performed using neat sulfatide without chemical modification.

 
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