ライフサイエンスコーパス: sulfatide

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 eramide (GalCer) and its sulfated derivative sulfatide.

8 rebroside (GalC) and its sulfated derivative sulfatide.

9 galactolipids galactocerebroside (GalC) and sulfatide.

10 there was an exceptionally strong binding to sulfatide.

11 rebroside (GalC) and its sulfated derivative sulfatide.

12 containing hydroxylated fatty acids and with sulfatide.

13 alter selectin binding to sLex, heparin, or sulfatide.

14 th micromolar affinities similar to that for sulfatide.

15 N-terminal domain binds liposomes containing sulfatide.

16 to the laminin coiled-coil dystroglycan and sulfatides.

17 of myelin 2-hydroxy galactosylceramides and -sulfatides.

18 responsible for the lysosomal hydrolysis of sulfatides.

19 by treatment of the substrate with SGGLs or sulfatides.

20 s for TSP1, heparan sulfate proteoglycan and sulfatides.

21 ng, including phospholipids, cholesterol and sulfatides.

22 eficient (ASA knockout) mice that accumulate sulfatides.

23 tides and 10 to 1,000 nM for C16:0 and C24:0 sulfatides.

24 was found to contain 17 gangliosides and 13 sulfatides.

25 lethanolamines, 2 phosphatidylinositols), 10 sulfatides (5 hydroxylated species and 5 nonhydroxylated

26 -[14C]arachidonoyl-phosphati dylethanolamine:sulfatide (70:0.2:30) were incubated with the supernatan

27 Neutrophils stimulated with sulfatide, a ligand for the L-selectin receptor, or the

28 ein for arylsulfatase A in the hydrolysis of sulfatide, a lipid component of myelin.

29 We now show that SC expression of galactosyl-sulfatide, a Lm-binding glycolipid, precedes that of Lms

30 We identified sulfatide, a major constituent of CNS myelin, as a novel

31 egulatory mechanism following recognition of sulfatide, a self-glycolipid ligand for a subset of CD1d

32 Sulfatide accumulated, but galactosylceramide remained a

33 loss of Sap B function leads to progressive sulfatide accumulation in satellite cells surrounding th

34 We show that sulfatide accumulation significantly impacts the formati

35 that these inclusion bodies corresponded to sulfatide accumulation.

36 We therefore suggest that sulfatides act as counterions for interstitial ammonium

37 ids (in particular galactocerebroside and/or sulfatide) act as sensors and/or transmitters of environ

38 e platelet surface, and platelets expressing sulfatides adhere to P-selectin.

39 NS-resident microglia, are inactivated after sulfatide administration, and mice deficient in type I N

40 vine submaxillary mucins, and the glycolipid sulfatide, all of which present multivalent sialylated a

41 Strikingly, we found that the glycolipid Ag sulfatide also localized almost exclusively to early end

42 such that it is able to adhere to heparin or sulfatide and can reduce P-selectin adherence to these l

43 in are important in 987P fimbrial binding to sulfatide and glycoprotein receptors, suggesting differe

44 Thus, autoimmune responses to sulfatide and other lipids are present in individuals wi

45 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

46 Moreover, 71 sulfatides and 59 polar phospholipids (phosphatidylserin

47 te that two classes of sulfated glycolipids, sulfatides and HNK-1-reactive sulfoglucuronylglycolipids

48 type II NKT cells recognizes myelin-derived sulfatides and is selectively enriched in the CNS tissue

49 The lectin domain of brevican binds sulfatides and SGGLs in a calcium-dependent manner as ex

50 Intact, full-length brevican also binds both sulfatides and SGGLs.

51 er beta2-glycoprotein I forms a complex with sulfatides and thereby becomes a target for anti-phospho

52 d by phosphatidylcholine, sphingomyelin, and sulfatides and were not substantially stimulated by cere

53 roteoglycan, 3-sulfated galactosyl ceramide (sulfatide), and heparin.

54 directed against galactocerebroside sulfate (sulfatide); and RMAb, which is directed against galactoc

55 a1 contains major binding sites for heparin, sulfatide, and alpha-dystroglycan and plays a critical r

56 amide, glucosylceramide, galactosylceramide, sulfatide, and globotriaosylceramide are abnormally incr

57 inding to collagen IV, to bind to galactosyl sulfatide, and to selectively convert alpha-short arm de

58 nd CHO cells expressing P-selectin adhere to sulfatides, and anti-P-selectin antibodies inhibit this

59 ones corresponding to phosphatidylinositols, sulfatides, and gangliosides were recorded in negative i

60 hosphoethanolamines, glycerophospho-serines, sulfatides, and gangliosides.

61 th diverse targets such as heparan sulfates, sulfatides, and integrins on cell surfaces.

62 hermore, both anti-P-selectin antibodies and sulfatide antagonist MCSP significantly reverse platelet

63 e data presented here indicate that GalC and sulfatide are essential in proper CNS node and paranode

64 Sulfatides are expressed on the platelet surface, and pl

65 blasts become competent for BM assembly when sulfatides are intercalated into their cell surfaces.

66 Sulfatides are most highly modulated by wild-type p53 tr

67 de carrier(s) in human CSF demonstrated that sulfatides are specifically associated with apoE-contain

68 Sulfatides are sulfated glycosphingolipids expressed on

69 Sulfatides are sulfated glycosphingolipids present on th

70 c phospholipids, as commonly known, but also sulfatides are targets for most anti-phospholipid antibo

71 Sulfated galactosylceramides (sulfatides) are glycosphingolipids associated with chole

72 ously that an antibody to galactocerebroside/sulfatide arrested terminal differentiation, suggesting

73 can powerfully inhibit axon growth, identify sulfatide as a novel myelin-associated axon growth inhib

74 Thus, we have identified sulfatide as a self-lipid recognized by human iNKT cells

75 Here, we show a novel role for sulfatides as a major ligand for P-selectin in platelet

76 mouse CD1d in complex with cis-tetracosenoyl sulfatide at 1.9 A resolution reveals that the longer ci

77 bound CD1d is inefficient in presenting lyso-sulfatide at neutral pH, it is efficiently presented at

78 The nonhydrolyzed sulfatide-Azure A is recovered and measured at a wavelen

79 total sulfatide used in the enzyme reaction (sulfatide-Azure A present in a parallel assay performed

80 rfaces decreased the immunoreactivity toward sulfatide-beta2-glycoprotein I complex by >50% in 12 of

81 Selective sulfatide binding may indicate possible function for GSD

82 ed by site-directed mutagenesis to study its sulfatide binding properties.

83 Dab2 sulfatide-binding motif contains two helices when embedd

84 e of a Dab2-derived peptide encompassing the sulfatide-binding motifs has been determined in dodecylp

85 surface by binding to sulfatides through two sulfatide-binding motifs, modulating the extent of plate

86 Both sulfatide micelles and sulfatide-binding recombinant malaria circumsporozoite p

87 son to other sulfatides or alphaGalCer, lyso-sulfatide binds with lower affinity to CD1d.

88 he role of MmpL8-mediated lipid transport in sulfatide biogenesis, we insertionally inactivated the m

89 SL-1 are coupled and that the final step in sulfatide biosynthesis may be the extra-cellular esterif

90 nct mode of recognition of a self-glycolipid sulfatide bound to CD1d by a type II NKT TCR.

91 et of anti-phospholipid antibodies, bound to sulfatide-bound beta2-glycoprotein I and previous absorp

92 antibodies from 4 of 5 patients reacted with sulfatide-bound beta2-glycoprotein I.

93 s a single species of sulfatide, namely lyso-sulfatide but not other sulfatides containing additional

94 CGT-deficient mice do not synthesize GalC or sulfatide but surprisingly form myelin containing glucoc

95 Beta2-glycoprotein I binds to surface-bound sulfatides but not to other glycolipids, such as ceramid

96 In addition, sulphogalactosylceramide (sulfatide) but not heparin can induce HPC mobilization.

97 JL/J mice with a synthetic cis-tetracosenoyl sulfatide, but not alpha-galactosylceramide, reverses on

98 Sulfatide, but not galactocerebroside or ceramide, stron

99 bited the binding of laminin to bovine brain sulfatide, but not to its cell surface receptors on MCF-

100 branes immobilized with phosphoinositides or sulfatide, but not with cardiolipin.

101 Since recognition of sulfatide by CD1d-restricted T cells has now been shown

102 ibly communicating with the sulfate group of sulfatide by hydrogen bonding and/or salt bridge formati

103 binding self-glycolipid ligands such as lyso-sulfatide can be presented via the secretory and endosom

104 er a single immunodominant form of synthetic sulfatide can treat ongoing chronic and relapsing EAE in

105 Examination of potential sulfatide carrier(s) in human CSF demonstrated that sulf

106 The sulfatide/CD1d-tetramer(+) cells isolated from naive mic

107 in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain li

108 At a sulfatide coating density of 1 microg/well, beta2-glycop

109 II NKT cell TCRs, therefore, recognize CD1d-sulfatide complexes by a distinct recognition mechanism

110 The increase in sulfatide concentration by a 14-mer prosaptide, TX14(A),

111 Herein prosaposin was found to increase sulfatide concentrations in primary and transformed Schw

112 posins, only saposin C was found to increase sulfatide concentrations in these cell types.

113 Sulfatides constitute a major component of myelin glycol

114 major myelin lipids galactosylceramides and sulfatides contain 2-hydroxy fatty acids.

115 lfatide, namely lyso-sulfatide but not other sulfatides containing additional acyl chains.

116 Reduced levels of binding to sulfatide-containing liposomes correlated with reduced f

117 mutant (K117A) did not interact at all with sulfatide-containing liposomes.

118 In contrast, the sulfatide content in brain tissues from human apoE4-expr

119 TX14(A) enhanced the sulfatide content of primary Schwann cells by 2.5-fold,

120 Renal sulfatide-deficient mice had lower urinary pH accompanie

121 Blocking sulfatide degradation from the saposin B deficiency dimi

122 We found profound inhibition of sulfatide-dependent T cell proliferation which was parti

123 Sulfatide derived from the myelin stimulates a distinct

124 Assembly is characterized by coalescence of sulfatide, DG, and c-Src into a Lm-associated complex; b

125 abrogate 987P binding to the lipid receptor sulfatide did not affect the interaction with the glycop

126 Mice unable to make sulfatide did not regenerate RGC axons more robustly aft

127 metachromatic leukodystrophy, who accumulate sulfatides due to a deficiency in arylsulfatase-A, direc

128 tail of CD1b to lysosomes, failed to present sulfatide efficiently.

129 reas other lipids, such as sphingomyelin and sulfatide, either did not affect ISVP* formation or prev

130 here, the histone H1 molecules stabilize the sulfatide-fimbriae interaction by simultaneously binding

131 onance shows that the affinity of human CD1d-sulfatide for the iNKT cell receptor is relatively low c

132 ce lacking the ability to synthesize GalC or sulfatide form dysfunctional and unstable myelin.

133 is obtained by subtracting the nonhydrolyzed sulfatide from the total sulfatide used in the enzyme re

134 by dextran sulfate 500K, dextran sulfate 5K, sulfatides, fucoidan, and heparin but not by chondroitin

135 ed by decreased brain levels of cholesterol, sulfatide, galactosylceramide, and triglyceride.

136 ed sphingolipid analogs of glucosylceramide, sulfatide, ganglioside GM1, ceramide 1-phosphate, sphing

137 matrix for imaging of acidic lipids such as sulfatides, gangliosides, and phosphatidylinositols in t

138 by 3'SL was least sensitive to inhibition by sulfatide, gastric mucin, and other sulfated oligosaccha

139 Here, we demonstrate that sulfatides, highly charged anionic glycosphingolipids, a

140 eature of neuroinflammatory disease and that sulfatide in APCs may contribute to the endogenous pathw

141 lted in decreased sulfate incorporation into sulfatide in cultures of differentiating OL.

142 Over 50% of GalCer and sulfatide in myelin is hydroxylated by the integral memb

143 NK T cell hybridomas is unable to recognize sulfatide in the presence of CD1d+ antigen-presenting ce

144 cell reactivity toward these GSLs and to the sulfatides in a fashion comparable with alpha-GalCer.

145 Sulfatides in brain lipid extract were also easily detec

146 esponsible for the catabolism and control of sulfatides in humans.

147 es a first step in understanding the role of sulfatides in regulating PDGFRalpha levels in OLs and it

148 This study points to a seminal role of sulfatides in renal ammonium handling, urinary acidifica

149 ts deficiency results in the accumulation of sulfatides in the cells of the central and peripheral ne

150 nse, suggesting an immunomodulatory role for sulfatides in the pathogenesis of tuberculosis.

151 ein I also depends on the coating density of sulfatides in the well.

152 icantly able to inhibit bacterial binding to sulfatide, indicating that in addition to glycoproteins,

153 elet mixture, reduces the number and size of sulfatide-induced aggregates.

154 PD-L pathway failed to prevent bacterial- or sulfatide-induced iNKT cell anergy, suggesting additiona

155 growth inhibitor, and provide evidence that sulfatide inhibition contributes to axon regenerative fa

156 Sulfatides interact with several cell adhesion molecules

157 oposed to play an essential role in the FasG-sulfatide interaction, possibly communicating with the s

158 These results show that sulfatide interactions with P-selectin are important in

159 The sulfatide interactions with P-selectin stabilize platele

160 stricted type II NKT cell subset reactive to sulfatide involved in the regulation of autoimmunity and

161 o than was wild-type myelin, indicating that sulfatide is a major component of the inhibitory activit

162 Presentation of lyso-sulfatide is inhibited in the presence of primaquine, co

163 The hydrolyzed sulfatide is monitored upon inclusion of the colorimetri

164 Thus, ARSA activity toward the sulfatide is obtained by subtracting the nonhydrolyzed s

165 Cis-tetracosenoyl sulfatide is one of the immunodominant species in myelin

166 We propose that sulfatide is recognized only by human iNKT cells because

167 g of polar lipids including gangliosides and sulfatides is a necessary step in understanding the dive

168 substrate, galactosyl-3-sulfate ceramide (or sulfatide), is performed using neat sulfatide without ch

169 caused an increase in brain cholesterol and sulfatide levels in four major brain structures (hippoca

170 sterol and establish that it does not affect sulfatide levels in the brain, these levels did increase

171 g high density lipoproteins, suggesting that sulfatide levels in the central nervous system (CNS) are

172 Excess hydroxy and non-hydroxy fatty acid sulfatide levels were present in brain and kidney.

173 Galactocerebroside and sulfatide, major galactosphingolipid components of oligo

174 urons and oligodendrocytes expressing the O4 sulfatide marker.

175 The sulfatide mass in hippocampus and cortex of apoE knockou

176 e that interactions of these antibodies with sulfatides may contribute to some of the clinical sympto

177 Sulfatide-mediated activation of type II NKT cells reduc

178 cells as well as after their inactivation by sulfatide-mediated activation of type II NKT cells.

179 ecause CD1 molecules are nonpolymorphic, the sulfatide-mediated immune-regulatory pathway can be targ

180 Protection from hepatic IRI by sulfatide-mediated inactivation of type I NKT cells was

181 The mechanism involved in sulfatide-mediated inhibition may share features with ot

182 Both sulfatide micelles and sulfatide-binding recombinant mal

183 specifically recognizes a single species of sulfatide, namely lyso-sulfatide but not other sulfatide

184 i-galactolipid antibodies, showing that anti-sulfatide O4 but not anti-galactocerebroside O1 blocks t

185 he 3-hydroxyl group in the sphingoid base of sulfatides offered some protection from oxidation for th

186 In this study, the effect of sulfatides on mouse T cell function and differentiation

187 The inhibitory effect of sulfatides on T cell function was CD1d-independent and w

188 sed sulfated content of galactosylceramides (sulfatides) on the regulation of PDGFRalpha in multipote

189 glucopyranosylceramide (beta-GlcCer) but not sulfatide or phospholipids in a CD1d-dependent manner, w

190 not involved in P-selectin binding to either sulfatide or sLeX.

191 In comparison to other sulfatides or alphaGalCer, lyso-sulfatide binds with low

192 erse lipids such as lysophosphatidylcholine, sulfatide, or mannosyl-phosophomycoketide, but not lipop

193 f MmpL8, which transports a precursor of the sulfatides, or MmpL11, which transports an unknown subst

194 receptor-activating peptide, suggesting that sulfatide-P-selectin interactions are necessary for the

195 These results indicate that GalC and sulfatide play important roles in myelin function and st

196 Cholesterol and sulfatides play many important roles in learning and mem

197 Immunization of mice with sulfatide plus myelin peptide resulted in a more severe

198 These structure and binding data on sulfatide presentation by CD1d have important implicatio

199 iNKT cells directly recognize myelin-derived sulfatide presented by CD1d.

200 ion reactive to a myelin-derived glycolipid, sulfatide, presented by CD1d.

201 ition of type I NKT cells by retinoids or by sulfatide prevents ALD.

202 Moreover, treatment of mice with sulfatide prevents antigen-induced experimental autoimmu

203 n of sulfatide-reactive type II NKT cells by sulfatide prevents induction of EAE.

204 elitis a model for human multiple sclerosis, sulfatide-reactive T cells but not invariant NK T cells

205 kine responses, we showed that activation of sulfatide-reactive type II NKT cells and plasmacytoid DC

206 We have shown that activation of sulfatide-reactive type II NKT cells by sulfatide preven

207 Collectively, the TCR repertoire of sulfatide-reactive type II NKT cells exhibits features o

208 We have shown that the activation of sulfatide-reactive type II NKT cells leads to a signific

209 IRI: type I NKT cells promote injury whereas sulfatide-reactive type II NKT cells protect against inj

210 ophosphatidylcholine (LPC) can stimulate the sulfatide-reactive type II NKT hybridoma Hy19.3 in a CD1

211 ate fimbrial binding to a glycoprotein and a sulfatide receptor on intestinal brush borders of piglet

212 ognized by human iNKT cells and propose that sulfatide recognition by innate T cells may be an import

213 y-determining region (CDR) loops, as well as sulfatide recognition separately encoded by nongermline

214 CD patient showed decreased cerebroside and sulfatide relative to normal white matter.

215 pe II NKT cells with antibody or the agonist sulfatide, respectively.

216 ctosylceramide and galactosylsphingosine and sulfatide, respectively.

217 malization of the ratio of long versus short sulfatides, restored PDGFRalpha levels, corrected its lo

218 TCR in complex with CD1d and the self-lipid sulfatide, revealing the unusual recognition of CD1d by

219 rain lipid metabolism (e.g., accumulation of sulfatides) seen in APOE-deficient mice, indicating func

220 al structure of human CD1a in complex with a sulfatide self antigen at a resolution of 2.15 A.

221 method to measure developmentally regulated sulfatide species (C16:0, C18:0, C24:1, and C24:0) in ce

222 ption of an analytical method to study these sulfatide species in raft and non-raft membranes and has

223 Although it is known that sulfatide species show heterogeneity in their fatty acid

224 All four sulfatide species were more abundant in raft membranes t

225 Sulfatide-specific antibodies were also detected in SJL/

226 disease course of EAE, and administration of sulfatide-specific antibody exacerbated EAE.

227 ntly presented sulfatide to CD1a-restricted, sulfatide-specific T cells.

228 sis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebros

229 was, however, a marked effect of apoE on the sulfatide (ST) content in both the brain and CSF.

230 e recently noted a profound decline in brain sulfatides (ST) in subjects who died with incipient deme

231 lycerol (PG), phosphatidylinositol (PI), and sulfatides (ST).

232 rest, ganglioside GM2, asialo-GM2 (GA2), and sulfatides (ST).

233 Sulfatide stimulation in vitro led to prominent suppress

234 Alcian blue positive (sulfatide) storage cells were found in the brain, spinal

235 y mimics that of the alkyl chain in the CD1a-sulfatide structure.

236 eramide, and the sulfated glycosphingolipids sulfatide, sulf-lactosylceramide, and sulf-globopentaosy

237 -3-sulfate-3-sulfohydrolase), which converts sulfatide (sulfogalactocerebroside) to galactocerebrosid

238 We disrupted sulfatide synthesis by a genetic approach along the enti

239 tivate ERKs, which is essential for enhanced sulfatide synthesis in Schwann cells.

240 The PACAP effect on sulfatide synthesis was fully reproduced in a cerebellar

241 lated from human cerebrospinal fluid carries sulfatide that can be captured by APCs and presented by

242 ickling may expose normally cryptic membrane sulfatides that could mediate this adhesive interaction.

243 With the exception of sulfatides, the invasion-inhibitory effect was not media

244 the platelet membrane surface by binding to sulfatides through two sulfatide-binding motifs, modulat

245 stigated presentation of the self-glycolipid sulfatide to a type II NKT cell that specifically recogn

246 ld-type CD1a molecules efficiently presented sulfatide to CD1a-restricted, sulfatide-specific T cells

247 se prevention correlates with the ability of sulfatide to suppress both interferon-gamma and interleu

248 it is not important for presentation of lyso-sulfatide to type II NKT cells.

249 possible function for GSDMB in the cellular sulfatide transport.

250 Moreover, tolerized DCs from sulfatide-treated animals can adoptively transfer protec

251 After deacylation of bovine brain sulfatide under mild alkaline conditions and reacylation

252 g the nonhydrolyzed sulfatide from the total sulfatide used in the enzyme reaction (sulfatide-Azure A

253 e Sphingomonas glycosphingolipids (GSLs) and sulfatide variants were shown to activate human NKT cell

254 Myelin in which sulfatide was lacking or blocked using specific antibodi

255 binding to heparin, alpha-dystroglycan, and sulfatides was dependent upon both shared and unique con

256 that CD1d presenting self-lipids, including sulfatide, was widely recognized by gut Vdelta1+ gammade

257 lin-associated lipids galactocerebroside and sulfatide were modestly reduced in Igf1(-/-) brains.

258 ically selective images for cerebrosides and sulfatides were successfully obtained.

259 sitols, phosphatidylinositol-phosphates, and sulfatides) were scrutinized on rat brain tissue section

260 pports adhesion of cells expressing SGGLs or sulfatides, which was inhibited by monoclonal antibodies

261 Consistent with colocalization of CD1a and sulfatide, wild-type CD1a molecules efficiently presente

262 mologous series of ceramide monohexoside and sulfatide with hydroxylated fatty acyl chains ranging fr

263 First, FasG attaches strongly to sulfatide with hydroxylated fatty acyl chains.

264 en embedded in micelles, reversibly binds to sulfatides with moderate affinity, lies parallel to the

265 mide (or sulfatide), is performed using neat sulfatide without chemical modification.