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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.
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
31 We now show that SC expression of galactosyl-sulfatide, a Lm-binding glycolipid, precedes that of Lms
33 egulatory mechanism following recognition of sulfatide, a self-glycolipid ligand for a subset of CD1d
35 loss of Sap B function leads to progressive sulfatide accumulation in satellite cells surrounding th
39 ids (in particular galactocerebroside and/or sulfatide) act as sensors and/or transmitters of environ
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
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
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
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
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
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
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
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
75 blasts become competent for BM assembly when sulfatides are intercalated into their cell surfaces.
77 de carrier(s) in human CSF demonstrated that sulfatides are specifically associated with apoE-contain
80 c phospholipids, as commonly known, but also sulfatides are targets for most anti-phospholipid antibo
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
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
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
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
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
107 et of anti-phospholipid antibodies, bound to sulfatide-bound beta2-glycoprotein I and previous absorp
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
113 JL/J mice with a synthetic cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses on
115 bited the binding of laminin to bovine brain sulfatide, but not to its cell surface receptors on MCF-
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
124 in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain li
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
129 Herein prosaposin was found to increase sulfatide concentrations in primary and transformed Schw
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
147 metachromatic leukodystrophy, who accumulate sulfatides due to a deficiency in arylsulfatase-A, direc
149 reas other lipids, such as sphingomyelin and sulfatide, either did not affect ISVP* formation or prev
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
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
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
163 M. pneumoniae bound to surfaces coated with sulfatide in a manner that was dependent on sulfatide co
165 eature of neuroinflammatory disease and that sulfatide in APCs may contribute to the endogenous pathw
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.
172 es a first step in understanding the role of sulfatides in regulating PDGFRalpha levels in OLs and it
174 ts deficiency results in the accumulation of sulfatides in the cells of the central and peripheral ne
177 icantly able to inhibit bacterial binding to sulfatide, indicating that in addition to glycoproteins,
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
182 oposed to play an essential role in the FasG-sulfatide interaction, possibly communicating with the s
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
191 by neuron- or glial-specific rescue, whereas sulfatide is principally expressed and functional in gli
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
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
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
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
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
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
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
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
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
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
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
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
259 sis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebros
261 e recently noted a profound decline in brain sulfatides (ST) in subjects who died with incipient deme
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
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.
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
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
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.
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
299 en embedded in micelles, reversibly binds to sulfatides with moderate affinity, lies parallel to the