ライフサイエンスコーパス: sulfation

1 osition (2-O-sulfation) and C6 position (6-O-sulfation).

2 reochemistry, chain lengths, and patterns of sulfation.

3 consistent with the dependence of 2OST on N-sulfation.

4 vailable at http://dlab.clemson.edu/research/Sulfation.

5 HA and emphasize a specific role of CS chain sulfation.

6 induced compensatory increases in N- and 6-O-sulfation.

7 n is toxic to tissue function independent of sulfation.

8 of potential proteins subjected to tyrosine sulfation.

9 , C5-epimerization is required for normal HS sulfation.

10 enotype is associated with abnormal GlcA 2-O-sulfation.

11 n selective addition of N-sulfate and/or 2-O sulfation.

12 elective O- and N-sulfation and selective de-sulfation.

13 orientation and an imbalance in chondroitin sulfation.

14 ic modified heparins with variable levels of sulfation.

15 noglycans that display a different degree of sulfation.

16 the HS 6-O-sulfotransferase hst-6 inhibit N-sulfation.

17 morphogenesis, particularly the role of 6-O sulfation.

18 in significantly increased N-, 2-O-, and 6-O-sulfation.

19 ional negative feedback between 2-O- and 6-O-sulfation.

20 ructures, with an absolute dependency on 6-O-sulfation.

21 ation sites, and a putative site of tyrosine sulfation.

22 is effect could be modulated by degree of HS sulfation.

23 he vitelline membrane undergo Pipe-dependent sulfation.

24 that the altered HS structure could boost CS sulfation.

25 of disaccharides having different levels of sulfation.

26 ran sulfate/chondroitin sulfate disaccharide sulfation.

27 inhibition of glycosaminoglycan synthesis or sulfation.

28 entage of nonvolatile material, or increased sulfation.

29 ther external sulfate levels or proteoglycan sulfation.

30 rong dependence on the pattern and extent of sulfation.

31 any distinct scaffolds and varying levels of sulfation.

32 hesis that 2-O-sulfation occurs prior to 6-O-sulfation.

33 -sulfation with modest changes in N- and 2-O-sulfations.

34 shown to be quite sensitive to the sites of sulfation (4-, 6-, or 4,6-) and easily distinguishable f

35 The effects of hst-2 and hst-6 on N-sulfation, 6-O-sulfation, and 2-O-sulfation appear large

36 Tyrosine sulfation, a well-characterized post-translation modific

37 eloped to determine the type and location of sulfation/acetylation modifications as well as uronic ac

38 We found that chondroitin sulfation across the proximal femur cartilage varied dra

39 d p38 cascades, suggesting that altering 3-O-sulfation affects FGFR2IIIb-mediated signaling.

40 eover, these data suggest manipulation of HS sulfation after CNS injury as a potential novel approach

41 ry binding site, O- and N-linked glycans and sulfation also contribute to the tensile strength of the

42 Loss of 6-O sulfation also disrupted normal positioning of centrosom

43 aran sulfate structure caused by increased N-sulfation and 6-O-sulfation of glucosamine units in resp

44 OST-deficient embryos have reduced GAG chain sulfation and are refractory to exogenous Wnt8 overexpre

45 t FGF2-induced proliferation is dependent on sulfation and can be inhibited by exogenously added hepa

46 HS is subject to regulated enzymatic sulfation and desulfation and an attractive, although no

47 The effects on N-sulfation and growth factor binding were confirmed bioch

48 resulted in a significant impairment of 2-O-sulfation and induced compensatory increases in N- and 6

49 nduced leukocytosis requires glucosamine 6-O-sulfation and is caused by blockade of L-selectin-, P-se

50 The post-translational modifications sulfation and phosphorylation pose special challenges to

51 ng and emerging evidence for the roles of PG sulfation and receptor interactions in determining how t

52 odifications such as regioselective O- and N-sulfation and selective de-sulfation.

53 Both the degree of sulfation and the structure of the carbohydrate backbone

54 roRNA-24 (miR-24) targets NDST1 to reduce HS sulfation and thereby the binding affinity of HS for VEG

55 N-Sulfation and tri-sulfation of heparan disaccharides wer

56 contrast, hse-5 stimulates both 2-O- and 6-O-sulfation and, hst-2 and hst-6 inhibit 6-O- and 2-O-sulf

57 The various sulfation and/or acetylation patterns on heparin impart

58 uired sulfation at both the C2 position (2-O-sulfation) and C6 position (6-O-sulfation).

59 fects of hst-2 and hst-6 on N-sulfation, 6-O-sulfation, and 2-O-sulfation appear largely dependent on

60 ith increased APAP clearance, increased APAP sulfation, and decreased formation of toxic APAP metabol

61 d to methoxy group removal of the phenols, O-sulfation, and photochemical unmasking of the cycloprope

62 is post-translationally modified by tyrosine sulfation, and the sulfated isoform is present outside t

63 e is no well-defined sequence motif for TPST sulfation, and the underlying determinants of TPST sulfa

64 tings for increasing limestone resistance to sulfation, and thus retarding gypsum formation under SO(

65 ork of enzymes that catalyze deacetylations, sulfations, and epimerizations in specific positions of

66 hst-6 on N-sulfation, 6-O-sulfation, and 2-O-sulfation appear largely dependent on hse-5 function.

67 of HS but lacks the alternating high and low sulfation architecture.

68 The amount and pattern of HS sulfation are key determinants for the assembly of the t

69 HST3), an enzyme that catalyzes proteoglycan sulfation, as a susceptibility gene for LDD.

70 In vitro sulfation assays showed alkyl and aryl substitutions to

71 1 and 2 (HS6ST-1 and HS6ST-2), which perform sulfation at 6-O position in glucosamine in HS, impact o

72 binding of HS20 to heparan sulfate required sulfation at both the C2 position (2-O-sulfation) and C6

73 Hs2st and Hs6st) mutants showed that loss of sulfation at one position is compensated by increased su

74 at one position is compensated by increased sulfation at other positions, supporting normal FGF sign

75 eparan sulfate chains is more important than sulfation at particular sites along the chains.

76 6-O-Sulfation at the glucosamine residue contributes to a wi

77 ss spectrometry identified sites of tyrosine sulfation at the middle and top of CDR H3; substitutions

78 Tyrosine sulfation at three positions in the CXCR4 N-terminus is

79 h modified heparin indicated that N- and 6-O-sulfation but not 2-O-sulfation is required for HCV infe

80 To verify the hypothesis that the degree of sulfation, but also the arrangement of sulfate groups al

81 colon along with a trend of higher bile acid sulfation by intestinal cells.

82 y role for remodelling (reduction) of HS 6-O-sulfation by OECs, compared with SCs, to suppress bounda

83 he natural abundance and functions of HS 3-O-sulfation by taking into consideration the negative impa

84 Inhibition of CCR2 sulfation, by growth of expressing cells in the presence

85 gulator decreases lipogenesis, and oxysterol sulfation can be a key protective regulatory pathway aga

86 to the mild phenotypes of Hsepi mutants: HS sulfation compensation and possible developmental roles

87 Thus, sulfation compensation depends on the coordinated activi

88 Here, we show that HS sulfation compensation rescues both Decapentaplegic and

89 -O-endosulfatase, as a novel component of HS sulfation compensation.

90 rolling heparan sulfate (HS) biosynthesis is sulfation compensation.

91 e V2 sulfotyrosines, enhancement of tyrosine sulfation decreased binding and neutralization of HIV-1

92 everal tissue sources, regardless of overall sulfation degree, indicating a common recognition patter

93 arides, we showed that chain length and high sulfation density are the most important determinants fo

94 ially modulated by patterns of glial cell HS sulfation, dependent on Sulf 1 and Sulf 2 expression, to

95 ndary formation, supporting a role for an HS sulfation-dependent FGF signaling mechanism via FGF rece

96 interactions between mucin and MAM(HS) in a sulfation-dependent manner.

97 Heparan sulfate (HS) 3-O-sulfation determines the binding specificity of HS/hepar

98 ed domains (NS domains) interrupted by lower sulfation domains.

99 mpounds and authentic heparin, indicative of sulfation-dominant and GAG sequence-dependent activities

100 The results provide clues to in vivo sulfation, DTD treatment, and cartilage growth.

101 Increasing GAG sulfation expands the pH range for binding.

102 ch upon further amidation, deprotection, and sulfation gave the targeted nonsaccharide activators.

103 enes Ndst1 and Ndst2 but not the 6-O and 2-O-sulfation genes Hs6st1, Hs6st2 and Hs2st.

104 enchymal expression of the heparan sulfate N-sulfation genes Ndst1 and Ndst2 but not the 6-O and 2-O-

105 xyl group of this motif is highly subject to sulfation/glucoronidation-based inactivation in humans;

106 on intact HS, specifically on the 2-O and N-sulfation groups.

107 zoa, produce HS but only chondroitin without sulfation has therefore been puzzling.

108 n leads to a (4)C(1)-chair, and (c) IdoA 2-O-sulfation (IdoA2S) stabilizes the (1)C(4) conformer.

109 Recent studies of PG sulfation illustrate the challenges of attributing biolo

110 te SulfoTransferase) based on loss of CS-4-O-sulfation in a C41C4.1 mutant and in vitro sulfotransfer

111 The proportion of N-acetylation and N-sulfation in both free HS and HSPG sugar chains were sig

112 ts a novel, regulatory function for tyrosine sulfation in collagen interaction and control of fibril

113 RB4EA12) showed significant increase in 6-O-sulfation in fibrotic kidney compared with the control.

114 taining IdoA2S and GlcNS6S, and that the 3-O-sulfation in GlcNS6S3S significantly enhances the bindin

115 inhibition of glycosaminoglycan synthesis or sulfation in HCT-8 cells.

116 published evidence indicating a role for 2-O sulfation in HGF binding, primary epithelial cells isola

117 dogenic peptide IAPP is dependent on overall sulfation in HS synthesized by beta-TC3 cells.

118 his result suggests that the increase in 6-O-sulfation in Hsepi mutants is critical for the rescue of

119 rating the importance of heparan sulfate 6-O sulfation in lacrimal gland FGF signaling.

120 he functional impact of site-specific glycan sulfation in modulating this lectin-glycan interaction,

121 investigate the role of heparan sulfate and sulfation in other settings not limited to infectious di

122 arin compounds indicated a requirement of 6O-sulfation in the growth and branching of the UB.

123 t binds strongly to sequences containing 3-O-sulfation in the internal limiting membrane (ILM) and in

124 ese results suggest an important role of 6-O-sulfation in the pathogenesis of fibrosis associated wit

125 sought to elucidate the role of variable HS sulfation in UB branching morphogenesis, particularly th

126 difications of the sugar moieties, including sulfations in specific positions.

127 t HCII, lacking N-glycosylation and tyrosine sulfation, inactivated alpha-thrombin with a 1:1 stoichi

128 Conversely, inhibition of tyrosine sulfation increased sensitivity to soluble CD4, 412d, an

129 pathway, acts as a positive regulator of HS-sulfation, increasing the N-sulfotransferase activity of

130 By disrupting (with sulfation inhibitors and heparinase) and partially recon

131 Tyrosine O-sulfation is a common protein post-translational modific

132 Tyrosine O-sulfation is a post-translational modification catalyzed

133 Tyrosine sulfation is a type of post-translational modification (

134 Tyrosine sulfation is an important post-translational modificatio

135 ur findings indicate that Ndst1-dependent HS sulfation is critical for mandibular and TMJ development

136 , we could unequivocally prove that tyrosine sulfation is critical for the potency of PG9 and RSH.

137 Proper sulfation is mediated by biosynthetic enzymes, including

138 for terrestrial plant/bacterial systems, but sulfation is not present in these cases, meaning the mar

139 The affinity of FGF2 for HS with reduced 6-O-sulfation is preserved, although FGFR1 activation is inh

140 icated that N- and 6-O-sulfation but not 2-O-sulfation is required for HCV infection and that the min

141 subcutaneous tumor nodules with reduced 6-O-sulfation is significantly delayed at the initial stages

142 sulfation of N-acetylglucosamine (GlcNAc-6-O-sulfation) is highly conserved in PNS myelin between the

143 of uronic acid epimers as well as geometric sulfation isomers.

144 The results reveal that SPGG's sulfation level moderately affected FXIa inhibition pote

145 Higher HS abundances and lower average sulfation level of HS were detected in glioblastoma (GBM

146 ay in angiogenic cytokine activation, HS 6-O-sulfation level, determined by the expression of HS6ST i

147 hamphetamine greatly increase HS content and sulfation levels in the lateral hypothalamus and that HS

148 Our data indicate that sulfation levels, chain length, and conformation all eff

149 n the two complexes provide insight into the sulfation mechanism for these substrates.

150 specifically examined the role of the HS 2-O sulfation modification on the morphogenetic capacity of

151 o be recognized by HS20 if an additional 3-O-sulfation modification was present.

152 was found to be more sensitive to the HS 6-O sulfation modification when compared to the 2-O sulfatio

153 fation modification when compared to the 2-O sulfation modification.

154 induction are markedly sensitive to the 2-O sulfation modification.

155 S oligosaccharides with distinct lengths and sulfation modifications.

156 ding molecules and, crucially, presented GAG sulfation motifs fundamental to mediating stem cell beha

157 /heparin through the presentation of defined sulfation motifs within polymeric scaffolds.

158 are modified in a complex manner by N- and O-sulfation, N-acetylation, and epimerization of the uroni

159 Depending on the degree of sulfation, next to the singly charged ionic species doub

160 active sulfate incorporation, explaining the sulfation normalization with age.

161 tive site supporting the hypothesis that 2-O-sulfation occurs prior to 6-O-sulfation.

162 mature active and inactive form, caused by a sulfation of a copper binding histidine.

163 lated MW 216 OSs, known to be formed through sulfation of C5-epoxydiols, second-generation gas-phase

164 In addition, sulfation of CCR5 is crucial for mediating interactions

165 While 4-O-sulfation of galactosamine dominated, we also detected 6

166 nds on 2-O-sulfation of uronic acids and 6-O-sulfation of glucosamine residues, we genetically ablate

167 ture caused by increased N-sulfation and 6-O-sulfation of glucosamine units in response to the decrea

168 N-Sulfation and tri-sulfation of heparan disaccharides were significantly in

169 evelopment, suggesting that both 2-O and 6-O sulfation of heparan sulfate contribute to FGF signaling

170 Specifically, altered sulfation of heparan sulfate in mutant neutrophils affec

171 prostate, pancreas), is in part dependent on sulfation of heparan sulfate proteoglycans.

172 ated DNA synthesis, even after inhibition of sulfation of heparan sulfate proteoglycans.

173 In this mutant, N-sulfation of heparan sulfate was disrupted after the len

174 mutations disrupted 2-O and/or 6-O but not N-sulfation of heparan sulfate.

175 3-O-Sulfation of HS is catalyzed by the 3-O-sulfotransferase

176 Increased sulfation of HS resulting from elevated HS 6-O-sulfotran

177 dominant monosaccharide sequence and reduced sulfation of HS, indicating that HS may interact differe

178 N-sulfotransferase 1 (Ndst1) that catalyzes sulfation of HS-PG glycosaminoglycan chains.

179 glycosaminoglycan (GAG), generated from the sulfation of hyaluronic acid, are anti-inflammatory but

180 usion, but we detected little to no tyrosine sulfation of IZUMO1 and found that IZUMO1 expression and

181 tes derived from metabolic hydroxylation and sulfation of LC-PCBs have been implicated in endocrine d

182 Thus, hydroxylation and sulfation of LC-PCBs result in selective interactions wi

183 rent efficiencies and how TPSTs catalyze the sulfation of multiple tyrosine residues in a substrate p

184 mouse PNS myelin, demonstrating that the 6-O-sulfation of N-acetylglucosamine (GlcNAc-6-O-sulfation)

185 nated axonal survival through the GlcNAc-6-O-sulfation of N-glycans on glycoproteins.

186 Cells deficient in enzymes involved in sulfation of proteins and proteoglycans showed strongly

187 Tyrosine sulfation of proteins is an important post-translational

188 es that catalyze post-translational tyrosine sulfation of proteins.

189 cartilage and bone and is important for the sulfation of proteoglycans such as aggregan.

190 inked galactose; a remarkable high degree of sulfation of such glycans was observed.

191 eparan sulfate oligomers, we identified that sulfation of the 3-OH position of N-sulfated glucosamine

192 il infiltration in mice in which the overall sulfation of the chains was reduced by selective inactiv

193 We have investigated the effect of tyrosine sulfation of the chemokine receptor CCR2 on its interact

194 Tyrosine sulfation of the chemokine receptor has been shown to be

195 In summary, these data demonstrate that the sulfation of the CS chain of bikunin and/or its core pro

196 , followed by a rearrangement and subsequent sulfation of the epoxy group in the particle phase.

197 iotechnological heparins derived by chemical sulfation of the Escherichia coli K5 polysaccharide reve

198 Sulfation of the GAG chain is key as evidenced by the re

199 ls and heparan sulfate and show that overall sulfation of the heparan sulfate chains is more importan

200 ring biosynthesis, greatly influencing total sulfation of the heparan sulfate chains.

201 nding to heparan sulfate and that N- and 6-O-sulfation of the heparan sulfate proteoglycans is requir

202 amydia strongly correlates with the level of sulfation of the host cell, not simply with the amount o

203 In addition we demonstrate that sulfation of this motif contributes to ligand internaliz

204 trometry to demonstrate that RaxST catalyses sulfation of tyrosine 22 of the Xoo Ax21 (activator of X

205 ine units in response to the decrease in 2-O-sulfation of uronic acid residues.

206 development and FGF signaling depends on 2-O-sulfation of uronic acids and 6-O-sulfation of glucosami

207 st (which encodes an enzyme required for 2-O-sulfation of uronic acids in heparan sulfate) did not in

208 se (Hs2st; an enzyme which catalyzes the 2-O-sulfation of uronic acids in heparan sulfate).

209 etermine neuronal preference toward specific sulfations of five CS variants: CS-A, CS-B (dermatan sul

210 Blocking sulfation on CD44s modestly decreases the tensile streng

211 The results highlight sulfation on the HIV co-receptor CCR5 and cellular aggre

212 Among these, the pattern of sulfation on the PG sugar chains is a paramount determin

213 ation factor V resulted in identification of sulfation on tyrosine 1513.

214 The results indicate that N-sulfation or a factor requiring N-sulfation regulates pr

215 ures of the glycosaminoglycans with variable sulfation or that the glycans are desulfated before clea

216 irement for N-linked glycosylation, tyrosine sulfation, or desensitization motifs but identified a re

217 iabetes appears to arise from accelerated de-sulfation, owing to the induction of a sulfatase.

218 data suggest that TPST-2-mediated tyrosine O-sulfation participates in regulating the sperm surface p

219 isaccharides to obtain information about the sulfation pattern and uronic acid epimerization.

220 of HS, which requires identification of the sulfation pattern as well as the uronic acid epimerizati

221 Sulf2, which remodel the heparan sulfate 6-O-sulfation pattern in the extracellular matrix.

222 activity of neutrophils is influenced by the sulfation pattern of heparan sulfate.

223 The sulfation pattern of IAPP-bound versus non-bound HS from

224 These features are independent of the sulfation pattern of the bulk HS chains.

225 The sulfation pattern of the heparan sulfate chains formed d

226 us system (CNS) are governed by the specific sulfation pattern on the glycosaminoglycan (GAG) chains

227 ition; tetrasaccharides lacking the specific sulfation pattern were found to preferentially bind CCL5

228 mating the extent of characterization of the sulfation pattern which is achieved by the set of measur

229 opose that either the sulfate groups (or the sulfation pattern) at the reducing end of the chondroiti

230 of aglycone affect the extent of sulfation, sulfation pattern, disaccharide composition, and chain l

231 aries with variations in glycan sequence and sulfation pattern.

232 the human retina, by both GAG chain type and sulfation pattern.

233 synthesis of oligosaccharides with different sulfation patterns and sizes from a disaccharide buildin

234 ned synthetic HS tetrasaccharides varying in sulfation patterns and uronic acid epimerization were an

235 HSPG activity is dictated by sulfation patterns controlled by sulfotransferases, whic

236 HEP-like trisaccharides harboring different sulfation patterns demonstrated that all of them bound t

237 y was employed to determine the quantity and sulfation patterns of circulating glycosaminoglycans.

238 Sulfation patterns of CS chains influence their interact

239 GlcAbeta(1 -->, where X stands for different sulfation patterns of fucose (X = 3,4S (46%), 2,4S (39%)

240 By controlling the sulfation patterns of heparan sulfate (HS) on pluripoten

241 the regulating role of NDST-1 in mapping the sulfation patterns of HS.

242 The sulfation patterns of these glycosaminoglycans are highl

243 to heparin octasaccharide isomers of varying sulfation patterns results in similar arrival time distr

244 octasaccharide structural isomers of various sulfation patterns were investigated using ion mobility

245 f attributing biological actions to specific sulfation patterns, and suggest ways in which highly sim

246 haride sequences decorated to give different sulfation patterns, which are termed here "wobble CS/DS

247 n sulfate oligosaccharides with well-defined sulfation patterns.

248 hromosomal protein methylation, acetylation, sulfation, phosphorylation).

249 We further showed that tyrosine sulfation plays a role in binding and neutralization.

250 However, the low natural abundance of HS 3-O-sulfation poses a serious challenge for functional studi

251 Variations in HS epimerization and sulfation provide enormous structural diversity, which i

252 Protein tyrosine sulfation (PTS) is a widespread posttranslational modifi

253 ine-3',5'-diphosphate, an end product of the sulfation reaction.

254 aled the catalytic mechanism of the tyrosine sulfation reaction.

255 e 5'-phosphosulfate (PAPS) is needed for all sulfation reactions in eukaryotes with implications for

256 adenosine 5'-phosphate (PAP), a byproduct of sulfation reactions utilizing the universal sulfate grou

257 (PAPS) is the high-energy sulfate donor for sulfation reactions.

258 Sulfation recodes the biologic activity of acceptors by

259 Genetic ablation of cell surface sulfation reduces bacterial adhesion and thereby alters

260 ate that N-sulfation or a factor requiring N-sulfation regulates primary and secondary branching even

261 Sulfotransferase (SULT)-mediated sulfation represents a critical mechanism in regulating

262 o suppress glycosaminoglycan substitution or sulfation, respectively.

263 on and, hst-2 and hst-6 inhibit 6-O- and 2-O-sulfation, respectively.

264 e technology and inhibitors of intracellular sulfation revealed the cooperative action of cell surfac

265 es and demonstrate that ventral proteoglycan sulfation serves as a positional cue for sea urchin skel

266 milar oligosaccharides with 2-O, 6-O and 3-O-sulfations showed inhibition for Wnt activation.

267 inst GAGs could be attributed to the GAG 6-O-sulfation site whereas only slip bond interaction can be

268 method to be useful in predicting potential sulfation sites and transferable to other TPST variants.

269 An unambiguous assignment of the sulfation sites becomes possible by subjecting sodium ad

270 Dissection of individual sulfation sites identified 2-O, 3-O-desulfated heparin (

271 Here, we localized the potential sulfation sites of Escherichia coli proteins on a proteo

272 d trideuteroperacetylation to label original sulfation sites with stable and hydrophobic trideuteroac

273 by allowing an unambiguous assignment of the sulfation sites.

274 Blocking HS sulfation specifically in the niche, termed the hub, led

275 ion, and the underlying determinants of TPST sulfation specificity remains elusive.

276 ffinity to the enzyme are important for TPST sulfation specificity, and their interplay results into

277 tructural and energetic determinants of TPST sulfation specificity.

278 HSulf-1 modulates the sulfation states of heparan sulfate proteoglycans critic

279 the Wg morphogen gradient by modulating the sulfation status of HS on the cell surface in the develo

280 precursor of all neurosteroids, via a single sulfation step and is present at low nanomolar concentra

281 Differences in the proportion of 6-O-sulfation suggest that 6-O-sulfotransferase and/or 6-O-s

282 blance to mutants with defective chondroitin sulfation suggesting tight developmental control of HA o

283 al features of aglycone affect the extent of sulfation, sulfation pattern, disaccharide composition,

284 ittermates in liver heparan sulfate content, sulfation, syndecan-1 protein levels, or affinity for he

285 e formation of fragment ions retaining their sulfation that arise from either cross-ring cleavages or

286 SULT1A1 and 2A1 catalyze the majority of sulfation that occurs during human Phase II metabolism.

287 primarily hexasaccharides with low degree of sulfation that were internal to the HS chains.

288 sis with the selectivity of enzyme-catalyzed sulfations, thus simplifying the overall synthetic opera

289 ions that block heparan sulfate synthesis or sulfation to compromise HSPG function.

290 on of these less-chlorinated PCBs, metabolic sulfation to form PCB sulfates is increasingly recognize

291 translational modification (PTM) of tyrosine sulfation to this neuropeptide was resolved.

292 ate for the first time that a combination of sulfation variants of CS chains without any protein comp

293 boundary-forming activity on high levels of sulfation was confirmed using a panel of semisynthetic m

294 osaminoglycans because it was abolished when sulfation was inhibited by chlorate treatment of the cel

295 agen fibril formation lag phase and tyrosine sulfation was required for this effect.

296 Chondroitin disaccharide sulfation was suppressed in all groups with respiratory

297 plays low constitutive levels of V2 tyrosine sulfation, which can be enhanced markedly by overexpress

298 proteins, and chondroitin chains, and their sulfation with 6-mum spatial resolution and without labe

299 f HS showed about 40% down-regulation in 6-O-sulfation with a parallel increase in iduronic acid mono

300 ide analysis showed considerably altered 6-O-sulfation with modest changes in N- and 2-O-sulfations.