ライフサイエンスコーパス: sulfo

1 escence response were synthesized based on 4-sulfo-1,8-naphthalic anhydride and a remarkable sensitiv

2 nches the fluorescence of N-iodoacetyl-N'-(5-sulfo-1-naphthyl)ethylenediamine (AEDANS) conjugated to

3 nyl)-4-methylcoumarin and N-iodoacetyl-N'-(5-sulfo-1-naphtyl)ethylenediamine has shown that the react

4 rp at position 264 and an N-iodoacetyl-N'-(5-sulfo-1-napthyl) ethylenediamine (AEDANS) moiety covalen

5 4-Methylumbelliferyl-6-sulfo-2-acetamido-2-deoxy derivatives of beta-D glucopyr

6 we examine the effect of PC, citrate, and n-sulfo-2-amino-tricarballylate (SAT, a PC analogue) on th

7 At 10(-3) M, a PC analogue, n-sulfo-2-aminotricarballylate and citrate also modulate t

8 CS pentasaccharides containing either a 6-O-sulfo-2-azidogalactosamine or a 6-O-sulfogalactosamine r

9 -7-[[[[5-hydroxy-6-[(4 cinnamylphenyl)azo]-7-sulfo-2-naphthalenyl]amino]-carbonyl]amino]-3-[(4-ci nna

10 luorophore pair IAEDANS [N'-iodoacetyl-N'-(1-sulfo-5-n-naphthyl)ethylenediamine]/DABMI [4-(dimethylam

11 cific fluorescent probe N-(iodoacetyl)-N'-(1-sulfo-5-naphthyl)ethylenediamine (IAEDANS).

12 tamide (IASL), N-[[(iodoacetyl)amino]ethyl]1-sulfo-5-naphthylamine (IAEDANS), and iodoacetamide (IAA)

13 o-alpha-d-glucopyranosyl-(1-->4)-2,3,6-tri-O-sulfo-alpha-d-gl ucopyranosyl-(1-->4)-2,3,6-tri-O-sulfo-

14 cid (the I ring) and 2-deoxy-2-sulfamido-6-O-sulfo-alpha-D-glucopyranosyl (the A ring).

15 t C-2 of one of the glucose moieties, 1-(2-O-sulfo-alpha-D-glucopyranosyl)-alpha-D-glycopyranose, was

16 -alpha-d-gl ucopyranosyl-(1-->4)-2,3,6-tri-O-sulfo-alpha-d-glucopyranosyl-(1-->4)-2,3,6-tri-O -sulfo-

17 ication of 3beta-cholestanyl 2,3,4,6-tetra-O-sulfo-alpha-d-glucopyranosyl-(1-->4)-2,3,6-tri-O-sulfo-a

18 ing copolymer comprised predominantly of 2-O-sulfo-alpha-L-iduronic acid (the I ring) and 2-deoxy-2-s

19 l type 1 but was 106% and 22% active with 3'-sulfo and 6-sulfo type 1, respectively.

20 In their oxidized sulfo and seleno forms, the P-diphenyl compounds are pre

21 annose, complex, and hybrid subtypes such as sulfo and sialyl forms.

22 ible and stochastic binding of heptakis-(6-O-sulfo)-beta-cyclodextrin and a nine base pair DNA hairpi

23 detection of a small molecule, heptakis(6-O-sulfo)-beta-cyclodextrin, are demonstrated.

24 nm, corresponding to the peptide YHP(p-[35S]sulfo-beta-aspartanilide)VPYVK, was observed in the chro

25 -alpha-d-glucopyranosyl-(1-->4)-2,3,6-tri-O -sulfo-beta-d-glucopyranoside, tridecasodium salt (PG545,

26 ptides containing a thioester handle using a sulfo-click linker is reported.

27 ere metabolized into a variety of gluco- and sulfo-conjugated metabolites.

28 ts, as well as N-acetylcysteine, taurine and sulfo-conjugates in both rats and humans.

29 e sulfotransferase (STD) is a hydroxysteroid sulfo-conjugating enzyme with preferential substrate spe

30 SULT2A1) is a cytosolic enzyme that mediates sulfo-conjugation of endogenous hydroxysteroids (dehydro

31 Furthermore, the sulfo-Cy5 labeled (R,R)-14 retained high agonist potency

32 (beta-D-gluco-4-enepyranosyluronic acid)-4-O-sulfo-D-galactose, and (3) 2-acetamido-2-deoxy-3-O-(beta

33 (beta-D-gluco-4-enepyranosyluronic acid)-6-O-sulfo-D-galactose, when treated with chondroitinase.

34 in bacteria, and the method uses a low cost sulfo donor, it can be readily utilized to synthesize la

35 ed to be the reaction products as follows; 5-sulfo-(E)-caftaric acid (a), 2-sulfo-(Z)-caftaric acid (

36 c acid (a), 2-sulfo-(Z)-caftaric acid (b), 2-sulfo-(E)-caftaric acid (c), (E)-caftaric acid-4-O-sulfa

37 Sulfo-EE(2) appears to be difficult to biotransform.

38 ed with the bifunctional cross-linking agent Sulfo-EGS (ethylene glycol bis (sulfosuccinimidylsuccina

39 FepA did not prevent modification of K483 by Sulfo-EGS but blocked its cross-linking to OmpF/C and Om

40 Site-directed mutagenesis determined that Sulfo-EGS reacted with two lysines, K332 and K483, and a

41 -ethylene glycol bis(succinimidylsuccinate) (sulfo-EGS), increasing the signal-to-noise ratio, minimi

42 thylene glycolbis(sulfosuccimidylsuccinate) (Sulfo-EGS), we studied conformational motion in the surf

43 atase, suggesting the presence of a critical sulfo ester in IRI.

44 e (PLL) layer with multiple binding sites by sulfo-ethylene glycol bis(succinimidylsuccinate) (sulfo-

45 o a single defined glycan, NeuAcalpha2-3(6-O-sulfo)Galbeta1-4[Fucalpha1-3]GlcNAc, also referred to in

46 ization of C-3 blocked compounds such as 3-O-sulfo-Galbeta1,3GalNAcbeta1,3Galalpha-OMe as acceptors b

47 Gal3ST-4 acted efficiently on Galbeta1,3(6-O-sulfo)GalNAcalpha-O-Al.

48 ing Gal beta 1,3GlcNAc beta-, Gal beta 1,3(6-sulfo)GlcNAc beta-, Gal beta 1,3GalNAc alpha-, Gal beta

49 ex, NeuAcalpha2-3Galbeta1-4[Fucalpha1-3](6-O-sulfo)GlcNAc) supported detectable binding.

50 Gal3ST-2 acted efficiently on Galbeta1,3(6-O-sulfo)GlcNAcbeta-O-Al, and Gal3ST-4 acted efficiently on

51 substrates: Gal3ST-3 utilized Galbeta1,4(6-O-sulfo)-GlcNAcbeta-O-Al as acceptor, Gal3ST-2 acted effic

52 Furthermore, a preexisting N-sulfo glucosamine residue prevents the action of NDST-1

53 , leading to the product with a cluster of N-sulfo glucosamine residues.

54 ves the linkage between a GlcA unit and an N-sulfo glucosamine unit carrying either a 3-O-sulfo or a

55 ase cleaves the linkage of a GlcA unit and N-sulfo glucosamine unit with a 2-O-sulfated GlcA residue,

56 ion of a glucosamine residue to form the 3-O-sulfo glucosamine, a structural motif critical for bindi

57 through detection of the NH resonances of N-sulfo-glucosamine residues.

58 volunteers were glucuronides, sulfates, and sulfo-glucuronides, and the total excretion of flavanone

59 luor 350, a coumarin derivative containing a sulfo group (i.e., bearing strong negative charge), show

60 kinetic studies showed that loss of the 3-O-sulfo group affected both the ability of the pentasaccha

61 strength and pH showed that loss of the 3-O-sulfo group caused a massive approximately 60% loss in b

62 block copolymers containing S-domains (high sulfo group content) placed adjacent to N-domains (low s

63 p content) placed adjacent to N-domains (low sulfo group content) were chemoenzymatically synthesized

64 2-O-sulfotransferase (HS-2OST) transfers the sulfo group from 3'-phosphoadenosine 5'-phosphosulfate (

65 These findings demonstrate that the 3-O-sulfo group functions as a key determinant of heparin pe

66 To elucidate the role of the 3-O-sulfo group in the activation mechanism, we compared the

67 This sulfo group interacts with the guanidinium group of Arg1

68 The location of the sulfo group of S-pyr is postulated to mimic the phosphon

69 to proceed through hydride transfer and the sulfo group of the oxidized and reduced molybdenum cente

70 (o) The enhancement of enzyme affinity by a sulfo group on C-6 of Gal was demonstrated by an increas

71 we compared the effects of deleting the 3-O-sulfo group or mutating the Lys(114) binding partner of

72 O-sulfotransferase (2OST) that transfers the sulfo group to the 2-OH position of iduronic acid (IdoA)

73 HS 2-O-sulfotransferase (2OST) transfers the sulfo group to the 2-OH-position of glucuronic or iduron

74 ferase (3-OST) is an enzyme that transfers a sulfo group to the 3-OH position of a glucosamine unit.

75 2-O-sulfotransferase (CS-2OST) transfers the sulfo group to the hexauronic acid that is adjacent to N

76 Alexa Fluor 350, a coumarin tag containing a sulfo group, along with guanidation of epsilon-amino gro

77 esults in up-regulation of 2-O-, 6-O-, and N-sulfo group-containing disaccharides, further emphasizin

78 ides and resistant tetrasaccharides with 3-O-sulfo group-containing glucosamine residues at their red

79 The content of 3-O-sulfo group-containing tetrasaccharides in a heparin cor

80 ne unit carrying either a 3-O-sulfo or a 6-O-sulfo group.

81 accharide sequence containing a critical 3-O-sulfo group.

82 The product ions resulting from the sulfo-group transfers were characterized by MS(3) experi

83 ified heparins showed that the presence of N-sulfo groups and either 2- or 6-O sulfo groups were requ

84 ght or more saccharide residues with seven O-sulfo groups and four N-sulfo groups exhibited potent in

85 osamine residue of heparan sulfate can carry sulfo groups at the 2-N, 3-O, and 6-O positions, leading

86 esidues with seven O-sulfo groups and four N-sulfo groups exhibited potent inhibition.

87 that a modest increase in the content of 3-O-sulfo groups in BIH increases the number of antithrombin

88 ethod for controlling the positioning of 6-O-sulfo groups in oligosaccharides.

89 determination of chain length and number of sulfo groups in the intact GAGs.

90 350, and Arg-190 of 2OST interact with the N-sulfo groups near the modification site, consistent with

91 ronic acid monosaccharides or the N- and 6-O-sulfo groups of the glucosamine sulfate monosaccharides.

92 ys-146, and Arg-147 from apoE and N- and 6-O-sulfo groups of the glucosamine units from the heparin f

93 dues make direct contact with either the 2-O-sulfo groups of the iduronic acid monosaccharides or the

94 drogen bonding distances to the carboxyl and sulfo groups of the uronic acid unit.

95 In contrast, 6-O-sulfo groups on HS are likely excluded by steric and ele

96 This requirement for the N-acetyl or N-sulfo groups on the glucosamine substrate can be explain

97 ementary to heparan sulfate rich in N- and O-sulfo groups such as that found in the liver and the bra

98 sence of N-sulfo groups and either 2- or 6-O sulfo groups were required for inhibition of toxicity.

99 Sulfo groups were transferred from adenosine 3'-phosphat

100 the detection and localization of the lost N-sulfo groups, potentially providing valuable insights in

101 g oligosaccharides with different numbers of sulfo groups.

102 on laser irradiation, reflecting lability of sulfo groups.

103 ated, in part, with the solvolytic loss of N-sulfo groups.

104 ride composition and content and position of sulfo groups.

105 onic acid linked to glucosamine carrying 6-O-sulfo groups.

106 oligosaccharides with precisely located 6-O-sulfo groups.

107 acid) linked to glucosamine carrying various sulfo groups.

108 sulfo-->6)GlcNAc, indicating that disulfated sulfo-->3Galbeta1-->4(sulfo-->6) GlcNAc-->R may be forme

109 HNK-1 glycan, sulfo-->3GlcAbeta1-->3Galbeta1-->4GlcNAc-->R, is uniquel

110 an is attached on core 2 branched O-glycans, sulfo-->3GlcAbeta1-->3Galbeta1-->4GlcNAcbeta1-->6(Galbet

111 The HNK-1 glycan, sulfo-->3GlcAbeta1-->3Galbeta1-->4GlcNAcbeta1-->R, is hi

112 eta1-->3Galbeta1-->4GlcNAcbeta1-->R, forming sulfo-->3GlcAbeta1-->3Galbeta1-->4GlcNAcbeta1-->R.

113 cating that disulfated sulfo-->3Galbeta1-->4(sulfo-->6) GlcNAc-->R may be formed by Gal3ST-3 in combi

114 , NeuNAcalpha2-->3Galbeta1-->4(Fucalpha1-->3(sulfo-->6))GlcNAcbeta1--> 3Galbeta1-->3GalNAcalpha1-->Se

115 ed core1 mucin-type O-glycan, Gal beta 1-->4(sulfo-->6)GlcNAc beta 1-->3Gal beta 1-->3GalNAc, as the

116 T-3 but not Gal3ST-2 can act on Galbeta1-->4(sulfo-->6)GlcNAc, indicating that disulfated sulfo-->3Ga

117 ver that of desulfo-hirudin, suggesting that sulfo-hirudin may offer clinical advantages for use as a

118 The affinity of sulfo-hirudin toward human thrombin is enhanced more tha

119 les direct expression in Escherichia coli of sulfo-hirudin, previously inaccessible through recombina

120 containing a glypican 5 core protein and 2-O-sulfo-iduronic acid residues at the nonreducing ends of

121 ceptors containing a glypican 5 core and 2-O-sulfo-iduronic acid to promote neural precursor prolifer

122 = 1.9 nM) as agonist, while corresponding p-sulfo isomer 6 (MRS5701) displayed mixed A1/A3AR agonism

123 r C-mannosyltryptophan, pseudouridine, and O-sulfo-L-tyrosine concentrations associated with incident

124 e show herein that the cell surface marker 6-sulfo LacNAc (slan) can define slan-positive CD14(+)CD16

125 6-Sulfo LacNAc DCs (slanDCs) are a major subpopulation of

126 6-sulfo LacNAc(+) DCs (slanDCs) represent a distinct popul

127 ying their cellular binding, we identified 6-sulfo LacNAc-expressing DCs (slanDCs) as having an outst

128 ha blockade during in vitro stimulation of 6-sulfo-LacNac DCs resulted in decreased production of IL-

129 alpha-producing myeloid subsets of CD14(-) 6-sulfo-LacNac(+) dendritic cells and CD14(+)CD16(+) "inte

130 tose but were not active with 2'- fucosyl-6'-sulfo lactose.

131 olated on sulfhydryl magnetic beads by using Sulfo-LC-SPDP.

132 use of the heterobifunctional cross-linker, Sulfo-LC-SPDP.

133 one and in complexes with 3'-NeuAc-Le(x), 3'-sulfo-Le(x) and 4'-sulfo-Le(x) have been determined at 1

134 s with 3'-NeuAc-Le(x), 3'-sulfo-Le(x) and 4'-sulfo-Le(x) have been determined at 1.95-2.1 A resolutio

135 ted hydrogen bond with the 4-OH of Gal in 3'-sulfo-Le(x), and forms a salt bridge with the sulfate gr

136 s a salt bridge with the sulfate group of 4'-sulfo-Le(x).

137 was treated with an intravenous infusion of Sulfo Lewis C after smoke exposure.

138 nificantly improved by the administration of Sulfo Lewis C.

139 FT IV showed great efficiency in forming 3'-sulfo Lewis x (249%) and Lewis x (345%) in mucin-type br

140 (e) 6'-Sulfo Lewis x and 3'-sialyl-6'-sulfo Lewis x (GLYCAM ligand) were not synthesized from

141 (e) 6'-Sulfo Lewis x and 3'-sialyl-6'-sulfo Lewis x (GLYCAM lig

142 , FT IV, and FT V formed 19%, 62%, and 47% 6-sulfo Lewis x as compared to Lewis x.

143 both peripheral node addressin and sialyl 6-sulfo Lewis X in high endothelial venules, considerably

144 Its epitope overlaps with sialyl 6-sulfo Lewis X, an L-selectin recognition determinant.

145 III and FT V formed approximately 4-fold 3'-sulfo Lewis x, as compared to 3'-sialyl Lewis x.

146 ligosaccharide, which overlaps with sialyl 6-sulfo Lewis X, the L-selectin recognition determinant.

147 Liposomes displaying 3'-sulfo Lewis(X)-like oligosaccharides, on the other hand,

148 sequences such as HNK-1, sulfo-Lewis(x), and sulfo-Lewis(a), in addition to glycosaminoglycans.

149 RANTES to sulfated sequences such as HNK-1, sulfo-Lewis(x), and sulfo-Lewis(a), in addition to glyco

150 rease in the order: homo- and arsonolipids < sulfo- < phosphono- < phospholipids.

151 O-Me] structures containing sialyl, fucosyl, sulfo, methyl, or fluoro substituents by identifying the

152 s, and MECA-79 antibody, which reacts with 6-sulfo N-acetyllactosamine on extended core 1 O-glycans.

153 Focused library development gave 3-sulfo-N-(4-aminobenzyl)-1,8-naphthalimide, potassium sal

154 -mannose-linked glycan structures, including sulfo-N-acetyllactosamine containing modifications.

155 3-Sulfo-N-benzyl-1,8-naphthalimide, potassium salt (25) wi

156 s achieved using a selective covalent label, sulfo-N-hydroxysuccinimide (NHSA).

157 decreased by 16-19% using EDC combined with sulfo-N-hydroxysuccinimide (s-NHS), and by 17-33% using

158 uccinimidyl iodo-acetate, suberic acid bis(3-sulfo-N-hydroxysuccinimide ester), suberic acid bis(N-hy

159 biotinylated with cell-impermeable reagents, sulfo-N-hydroxysuccinimide-biotin and sulfo-N-hydroxysuc

160 ins were labeled with the impermeant reagent sulfo-N-hydroxysuccinimide-biotin, both PrPC and PrPSc w

161 gents, sulfo-N-hydroxysuccinimide-biotin and sulfo-N-hydroxysuccinimide-S-S-biotin in the absence and

162 l-3-(3-dimethylaminopropyl)-carbodiimide and sulfo-N-hydroxysuccinimide.

163 The membrane-impermeable sulfo-N-hydroxysuccinimidyl (NHS) ester of oleate (SSO)

164 arried out over a range of concentrations of sulfo-N-succinimidyl acetate (SNSA).

165 e plasma membrane-impermeable CD36 inhibitor sulfo-N-succinimidyl oleate (20 muM) decreased lipolysis

166 quently decreased by the addition of BLT1 or sulfo-N-succinimidyl oleate (CD36 inhibitor), respective

167 ing with the spin-labeled reagent BSSDA [bis(sulfo-N-succinimidyl)doxyl-2-spiro-5'-azelate].

168 the heterobifunctional cross-linking reagent sulfo-N-succinimidyl-4-(fluorosulfonyl)benzoate, and the

169 ed by cell treatment with the CD36 inhibitor sulfo-N-succinimidyl-oleate.

170 roxysulfate radical, superoxide radical, and sulfo-NAD(P) in the mechanism of STAR toxicity and flavo

171 l-3-yl)piperidin-1-yl]butyl]benzothiophene-2-sulfo namide (72) was characterized in vitro on 14 targe

172 ion, the peptide analyte ions and the NHS or sulfo-NHS based reagent form a long-lived complex, which

173 tion, egg surface proteins were labeled with sulfo-NHS biotin, treated with PI-PLC, and analyzed by t

174 As the NHS or sulfo-NHS group leaves, an amide bond is formed between

175 Subsequent activation of the NHS or sulfo-NHS loss product ions results in sequence informat

176 -reagent complex results in a neutral NHS or sulfo-NHS molecule loss, which is a characteristic signa

177 Using EDC and Sulfo-NHS, terminal carboxyl groups of N-succinyl-Ala-Al

178 roteins at the plasma membrane compared to a sulfo-NHS-activated biotinylation or two-step SEEL.

179 odified by using a cell-impermeable reagent (sulfo-NHS-biotin), and then they are isolated via a liqu

180 lamine, iodoacetyl-LC-biotin, NHS-LC-biotin, sulfo-NHS-LC-biotin, and biotin-LC-hydrazide.

181 Twelve lysine residues were accessible to sulfo-NHS-LC-biotin.

182 chaffeensis, membrane-impermeable, cleavable Sulfo-NHS-SS-Biotin was used to label intact bacteria.

183 l-2-[biotinamido]ethyl-1,3-dithiopropionate (Sulfo-NHS-SS-Biotin), was used to label intact bacteria.

184 e at the resolution of the map, we used Mono-Sulfo-NHS-Undecagold labeling to increase preferentially

185 bined data reveal that this type of naphthyl-sulfo (NS) molecule directly targets the substrates but

186 the ability to synthesize highly purified N-sulfo-oligosaccharides having up to 21 saccharide residu

187 (j) FT III did not act on 6'-sulfo or 6'-sialyl type 1 but was 106% and 22% active wi

188 sulfo glucosamine unit carrying either a 3-O-sulfo or a 6-O-sulfo group.

189 nidinium with a few of 10 negatively charged sulfo or carboxyl groups of Arixtra at the interfaces.

190 etrazolium salt (2,3-bis(2-methoxy-4-nitro-5-sulfo-phenyl)-2H-tetrazolium-5-carboxanilide) to water-s

191 ar characterization of structurally defined, sulfo-phenylated, oligo- and polyphenylenes that incorpo

192 ydrolysis of aqueous dispersions of arsono-, sulfo-, phosphono- and phospholipids by phospholipase A2

193 l-6-(4-azido-2-nitrophenyl-amino) hexanoate (sulfo-SANPAH).

194 roteins off the surface of gels coated using sulfo-SANPAH, which corresponds to lower values of tract

195 aB3-peptide binding sites were identified by sulfo-SBED (sulfosuccinimidyl-2-[6-(biotinamido)-2-{p-az

196 coimmunoprecipitation studies combined with sulfo-SBED-biotin-transfer provided evidence for a direc

197 hemistry toolbox here with a second reagent, sulfo-SBP (benzophenone).

198 obifunctional photoactivatable cross-linker, sulfo-SDA (diazirine), has yielded high-density data tha

199 e unusual sulfated tetrasaccharide epitope 6-sulfo sialyl Lewis x (Siaalpha2-->3Galbeta1-->4[Fucalpha

200 ectin ligand sulfotransferase (LSST) forms 6-sulfo sialyl Lewis x (sLe(x)) on both core 2 branch and

201 results, we propose possible pathways for 6-sulfo sialyl Lewis x biosynthesis and suggest that sulfa

202 e the critical function of N-glycan-linked 6-sulfo sialyl Lewis X in L-selectin-dependent lymphocyte

203 dentified a class of N-glycans bearing the 6-sulfo sialyl Lewis X L-selectin ligand in high endotheli

204 3GlcNAcT) enabled the construction of the 6-sulfo sialyl Lewis x on extended core1 O-glycans, recapi

205 on lymphocytes and the carbohydrate ligand 6-sulfo sialyl Lewis X on high endothelial venules.

206 rbohydrate structural analysis showed that 6-sulfo sialyl Lewis X, a dominant ligand for L-selectin,

207 This epitope overlaps with 6-sulfo sialyl Lewis x, a recognition determinant for L-se

208 n in complex with its prime glycan target 6'-sulfo sialyl Lewis(x) A canonical motif for sialic acid

209 ed LSST, that directs the synthesis of the 6-sulfo sialyl Lewis(x) on L-selectin counterreceptors CD3

210 In contrast, 6-sulfo sialyl Lex containing a sulfate group on the N-ace

211 These combined results suggest that 6'-sulfo sialyl Lex is a much better ligand than sialyl Lex

212 HO cells expressing 6'-sulfo sialyl Lex or 6-sulfo sialyl Lex on their cell surface were tested for a

213 The resultant CHO cells expressing 6'-sulfo sialyl Lex or 6-sulfo sialyl Lex on their cell sur

214 The results indicate that 6'-sulfo sialyl Lex supports L-selectin-mediated adhesion m

215 CHO cells were incubated with synthetic 6'-sulfo sialyl Lex, NeuNAcalpha2-->3(sulfate-6)Galbeta1-->

216 te-6)Galbeta1-->4(Fucalpha1-->3) GlcNAc or 6-sulfo sialyl Lex, NeuNAcalpha2-->3Galbeta1-->4[(Fucalpha

217 ,3-fucosylated glycan receptors, including 6-sulfo-sialyl Lewis x (6-sulfo-sLe(x)).

218 Strikingly, bonds between L-selectin and 6-sulfo-sialyl Lewis X were impervious to ramp rate change

219 ut not for a sulfated-glycan binding site (6-sulfo-sialyl Lewis x) on peripheral node addressin.

220 ntified SIGNR7 binds preferentially to the 6-sulfo-sialyl Lewis(x) oligosaccharide, whereas SIGNR2 bi

221 with higher affinity than does sLe(x) or 6'-sulfo sLe(x) and that sulfation of sLe(x) capping groups

222 fact that L-selectin ligands that contain 6-sulfo sLe(x) are reduced at HEV.

223 Our results suggest that 6-sulfo sLe(x) binds to L-selectin with higher affinity th

224 ause beads coated with the selectin ligand 6-sulfo sLe(x) bound to trophoblasts, and trophoblasts bou

225 vidence has identified the contribution of 6-sulfo sLe(x) carried on N-glycans to lymphocyte homing i

226 nts as a result of significantly decreased 6-sulfo sLe(x) on HEV L-selectin counterreceptors, relativ

227 carbohydrates, we found that CL40 bound to 6-sulfo sLe(x) structures, on both core 2 and extended cor

228 6-Sulfo sLe(x), a sulfated carbohydrate determinant for L-

229 t cells, but a monoclonal antibody against 6-sulfo-sLe(x) fails to inhibit AmOmpA adhesion and A. mar

230 ceptors, including 6-sulfo-sialyl Lewis x (6-sulfo-sLe(x)).

231 didate contributors to the biosynthesis of 6-sulfo sLex in the context of L-selectin ligands.

232 PSGL-1 lacks 6-sulfo-sLex but contains sulfated tyrosine residues (Tyr-

233 In contrast, sLex and 6-sulfo-sLex did not support any Siglec-8 binding at the h

234 Whereas surfaces derivatized with sLex and 6-sulfo-sLex failed to support detectable Siglec-8 binding

235 signals at immobilized concentrations of 6'-sulfo-sLex of <5 pmol/spot.

236 d to support detectable Siglec-8 binding, 6'-sulfo-sLex supported significant binding with a Kd of 2.

237 e structures (6-sulfated sialyl Lewis x or 6-sulfo-sLex) as a recognition determinant within their he

238 ctin binds to the sulfated sialyl Lewis x (6-sulfo-sLex) epitope present on O-glycans of various glyc

239 e on the 6-position of the GlcNAc residue (6-sulfo-sLex, NeuAcalpha2-3Galbeta1-4[Fucalpha1-3](6-O-sul

240 Ac, also referred to in the literature as 6'-sulfo-sLex.

241 lly conjugated with T3 using a non-cleavable sulfo-SMCC linker.

242 nal chemical cross-linking reagents, BS3 and sulfo-SMPB, respectively, as well as glutaraldehyde and

243 ied structures containing 3-O-fucosyl or 6-O-sulfo substituents in the N-acetylglucosamine residues.

244 compared to the conventional method of using sulfo-succinimidyl-6-(4-azido-2-nitrophenyl-amino) hexan

245 rating chemical synthesis and two types of O-sulfo transferases, seven different hexasaccharides were

246 was 106% and 22% active with 3'-sulfo and 6-sulfo type 1, respectively.

247 on consist of five acidic residues and three sulfo-Tyr residues, thus representing a high density of

248 as follows; 5-sulfo-(E)-caftaric acid (a), 2-sulfo-(Z)-caftaric acid (b), 2-sulfo-(E)-caftaric acid (