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 on in which the nitrogen of the C-terminal N-sulfo-2,3-diaminopropionate residue attacks its thioeste

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

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

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

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

10 -7-[[[[5-hydroxy-6-[(4 cinnamylphenyl)azo]-7-sulfo-2-naphthalenyl]amino]-carbonyl]amino]-3-[(4-ci nna

11 3-O-sulfo (3-O-S) modification of HS has been linked to AD t

12 The reduced content of N-sulfo, 3-O-sulfo glucosamine, the central and critical r

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

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

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

16 the condensation of acyl-ACP and cysteate (3-sulfo-alanine) to form 3-ketocapnine.

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

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

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

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

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

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

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

24 droxylated metabolites and the corresponding sulfo and glucuronide conjugates.

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

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

27 not only expresses vertebrate motifs such as sulfo- and sialyl-Lewis A epitopes but displays a high d

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

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

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

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

32 namely, a 3'-sulfolactose derivative and 3'-sulfo-beta-galactosylceramide, have been accomplished.

33 The chemistry of sulfo-bromination of metals leading to dual-tapered 2D-s

34 The sulfo-bromination process is initially nucleated on the

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

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

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

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

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

40 e excimer-forming pyrene pair as a donor and sulfo-Cy3 dye as an acceptor, which demonstrated remarka

41 monstrated remarkable 75-fold enhancement of sulfo-Cy3 fluorescence upon target capturing.

42 involved in the resonance energy transfer to sulfo-Cy3.

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

44 drophobic cargo (Cy7) and hydrophilic cargo (Sulfo-Cy5) were successfully encapsulated in the PTA-Ps.

45 -I&T-based hybrid tracer, PSMA-I&F (DOTAGA-k(Sulfo-Cy5)-y-nal-k-Sub-KuE), has been developed and eval

46 ty (5-TAMRA-labeled ligand 19: K(i) 0.14 nM, sulfo-Cy5-labeled probe 21: K(i) 0.094 nM) and high stab

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

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

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

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

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

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

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

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

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

56 ene glycol bis(sulfosuccinimidyl succinate) (sulfo-EGS) cross-linker anions enable covalent cross-lin

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

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

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

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

61 In particular, the branched Neu5Aca2-3(6-O-sulfo)GalB1-4GlcNAc (6'-Su-SLacNAc) epitope was discover

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

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

64 -N-(2-naphthyl-sulfonyl)-Neu5Acalpha2-3-[6-O-sulfo]-Galbeta1-4GlcNAc (6'-O-sulfo (NSA)Neu5Ac) combine

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

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

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

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

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

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

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

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

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

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

75 The reduced content of N-sulfo, 3-O-sulfo glucosamine, the central and critical residue in h

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

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

78 sulting compounds were acylated to provide 3-sulfo-glucuronyl- and glucuronyl-containing glycosphingo

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

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

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

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

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

84 2-O-sulfotransferase (HS-2OST) transfers the sulfo group from 3'-phosphoadenosine 5'-phosphosulfate (

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

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

87 This sulfo group interacts with the guanidinium group of Arg1

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

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

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

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

92 s finding showed that LGS1 in sorghum uses a sulfo group to catalyze leaving of a hydroxyl group and

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

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

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

96 2-O-sulfotransferase (CS-2OST) transfers the sulfo group to the hexauronic acid that is adjacent to N

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

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

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

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

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

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

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

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

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

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

107 Moreover, we showed that one of the three sulfo groups can be easily substituted with S-, N-, and

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

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

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

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

112 350, and Arg-190 of 2OST interact with the N-sulfo groups near the modification site, consistent with

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

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

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

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

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

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

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

120 nclude that mutant 3-OST-6 fails to transfer sulfo groups to the 3-OH position of HS, resulting in in

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

122 Sulfo groups were transferred from adenosine 3'-phosphat

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

124 acid) linked to glucosamine carrying various sulfo groups.

125 g oligosaccharides with different numbers of sulfo groups.

126 on laser irradiation, reflecting lability of sulfo groups.

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

128 ride composition and content and position of sulfo groups.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 = 1.9 nM) as agonist, while corresponding p-sulfo isomer 6 (MRS5701) displayed mixed A1/A3AR agonism

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

147 ophosphocholines with Alzheimer's disease, O-sulfo-L-tyrosine with Parkinson's disease, glycine, xant

148 The 6-sulfo LacNAc (slan) antigen identifies a subset of non-c

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

150 6-Sulfo LacNAc DCs (slanDCs) are a major subpopulation of

151 6-sulfo LacNAc(+) DCs (slanDCs) represent a distinct popul

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

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

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

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

156 were mixed separately with the cross-linker (Sulfo-LC-SPDP) to enhance the immobalization of the anti

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

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

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

160 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

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

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

163 requires a tailored N-sulfoheparosan with N-sulfo levels similar to those of porcine heparins.

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

165 nificantly improved by the administration of Sulfo Lewis C.

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

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

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

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

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

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

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

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

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

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

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

177 se of their structural similarity and facile sulfo losses during analysis.

178 ty spectrometry (gated-TIMS) with negligible sulfo losses.

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

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

181 bility resolution and preservation of labile sulfo modifications afforded by gated-TIMS MS analysis a

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

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

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

185 3-Sulfo-N-benzyl-1,8-naphthalimide, potassium salt (25) wi

186 s, including those highly branched nonsialyl sulfo-N-glycans bearing lactosaminic extensions in both

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

208 RS-CoV-2 Spike Protein via the classical EDC/sulfo-NHS procedure.

209 ngly deprotonated N-hydroxysulfosuccinimide (sulfo-NHS)-based cross-linker anions are restricted to a

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

211 ification of lysine residues on the RBD with sulfo-NHS-acetate ablated binding to LRP1.

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

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

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

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

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

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

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

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

220 The ligand 6'-O-sulfo (NSA)Neu5Ac was conjugated to lipids for display o

221 calpha2-3-[6-O-sulfo]-Galbeta1-4GlcNAc (6'-O-sulfo (NSA)Neu5Ac) combined the lead 2-naphthyl sulfonyl

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

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

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

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

226 s this critical gap by identifying methyl 2-(sulfo-oxy)benzoate as a novel biomarker for distinguishi

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

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

229 We propose the use of the sulfo-phospho-vanillin assay (SPVA), a total lipid color

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

231 introduces new fluorescent properties to the sulfo-pillar[6]arene family via an incorporated p-terphe

232 The parent sulfo-pillar[6]arene is a high-affinity host with the po

233 Herein, we report the synthesis of extended sulfo-pillar[6]arenes (sP6), a new host class with a ped

234 The new extended sulfo-pillar[6]arenes have either a monodirectional (A1s

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

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

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

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

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

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

241 using sulfosuccinimidyl 4,4'-azipentanoate (sulfo-SDA) with our recently developed data-independent

242 A Sulfo-SIAB linker yielded superior results over an SM(PE

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

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

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

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

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

248 3GlcNAcT) enabled the construction of the 6-sulfo sialyl Lewis x on extended core1 O-glycans, recapi

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

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

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

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

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

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

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

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

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

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

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

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

261 ,3-fucosylated glycan receptors, including 6-sulfo-sialyl Lewis x (6-sulfo-sLe(x)).

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

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

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

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

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

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

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

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

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

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

272 6-Sulfo sLe(x), a sulfated carbohydrate determinant for L-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

289 Accordingly, we first prepared a SULFO-TAG labeled conjugate of recombinant Protein-A/G t

290 imized direct binding assay design employing SULFO-TAG labeled Protein-A/G represents a useful analyt

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

292 cid based on using recombinant glycosyl- and sulfo-transferases.

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

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

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