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 hydroxylation, Hyp glycosylation, and/or Tyr sulfation.

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

4 noglycans that display a different degree of sulfation.

5 protein currently known to recognize HS 3-O-sulfation.

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

7 that the altered HS structure could boost CS sulfation.

8 of disaccharides having different levels of sulfation.

9 ran sulfate/chondroitin sulfate disaccharide sulfation.

10 inhibition of glycosaminoglycan synthesis or sulfation.

11 entage of nonvolatile material, or increased sulfation.

12 ther external sulfate levels or proteoglycan sulfation.

13 rong dependence on the pattern and extent of sulfation.

14 any distinct scaffolds and varying levels of sulfation.

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

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

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

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

19 n is toxic to tissue function independent of sulfation.

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

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

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

23 rides that differ in the pattern of N- and O-sulfation.

24 orientation and an imbalance in chondroitin sulfation.

25 se, and GLCE, an epimerase that promotes 6-O-sulfation.

26 lfotransferase integral to glycosaminoglycan sulfation.

27 hydrate extensively modified by differential sulfation.

28 (LacdiNAc) extensively modified by terminal sulfation.

29 reochemistry, chain lengths, and patterns of sulfation.

30 of potential proteins subjected to tyrosine sulfation.

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

32 molecular function of a specific form of HS sulfation, 2-O HS sulfation catalyzed by the enzyme Hs2s

33 ned HS oligosaccharides show that a rare 3-O-sulfation (3-O-S) of HS significantly enhances tau bindi

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

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

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

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

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

39 ons differentiated the 6-O sulfation and 3-O sulfation, allowing unambiguous structural assignment.

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

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

42 ostic cross-ring ions differentiated the 6-O sulfation and 3-O sulfation, allowing unambiguous struct

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 post-translationally modified by tyrosine O-sulfation and contribute to binding to collagen.

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

48 The sulfation and desulfation reactions modifying a variety

49 saccharide mixtures with a varying extent of sulfation and even for the determination of both predomi

50 The high degree of sulfation and fucosylation parallels the modifications o

51 Blocking sulfation and glycosaminoglycan synthesis reduces TcdA b

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

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

54 ed with the most pronounced effects, whereas sulfation and methoxylation of PCBs resulted in diminish

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

56 anslational modifications including tyrosine sulfation and proline hydroxylation within, and proteoly

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

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

59 th previous reports by others, we found that sulfation and sialylation drastically alter the MS(2) fr

60 erentiate them from Hp (particularly reduced sulfation and sulfated disaccharide content), and that t

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

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

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

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

65 esence of a 3,6-anhydro-bridge (LA unit) and sulfations and methylation).

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

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

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

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

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

71 nce is sustained over hydrothermal aging and sulfation as a result of highly dispersed and isolated a

72 postinfarction angiogenesis and identify HS sulfation as a therapeutic target for ischemic tissue re

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

74 1 and 2 (HS6ST-1 and HS6ST-2), which perform sulfation at 6-O position in glucosamine in HS, impact o

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

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

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

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

79 y of heparan sulfate for BDNF increased with sulfation at the 2-O position of iduronic acid and the N

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

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

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

83 methods for the characterization of protein sulfation by sulfopeptide enrichment are currently limit

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

85 Reported here is a general approach to O-sulfation by the sulfur(VI) fluoride exchange (SuFEx) re

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

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

88 yl carbonate (Fmoc), different patterns of O-sulfation can be installed.

89 n of a specific form of HS sulfation, 2-O HS sulfation catalyzed by the enzyme Hs2st, in midline astr

90 sulfated oligosaccharides for unlocking the "sulfation code" and understanding the roles of specific

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

92 Thus, sulfation compensation depends on the coordinated activi

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

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

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

96 As both carbohydrate density and degree of sulfation decrease with age in Bruch's membrane of the m

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

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

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

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

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

102 utations of host factors involved in heparan sulfation, endocytosis, endoplasmic reticulum processing

103 Our work demonstrates that this rare 3-O-sulfation enhances tau-HS binding and likely the transce

104 Chemical de-N-acetylation, chemical N-sulfation, enzymatic epimerization, and enzymatic sulfat

105 Increasing GAG sulfation expands the pH range for binding.

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

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

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

109 TcdA recognizes the sulfation group in sGAGs.

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

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

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

113 growth factor 2, showing that changes in 6-O-sulfation impact a key cartilage signaling pathway.

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

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

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

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

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

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

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

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

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

123 s also altered, with increased levels of 6-O-sulfation in osteoarthritic samples, which correlated wi

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

125 Mechanistically, both Sulfs reduced HS sulfation in the infarcted myocardium, thereby diminishi

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

127 Enhanced 3-O-sulfation increased binding to antithrombin, which enhan

128 Sulfation increased mesotrypsin activity but accelerated

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

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

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

132 O-sulfation is an important chemical code widely existing

133 Tyrosine sulfation is an important post-translational modificatio

134 Protein tyrosine O-sulfation is an important post-translational modificatio

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

136 The increased Sdc2 HS chains 6-O sulfation is driven by a specific N-terminal domain sequ

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 rences are due to a significantly higher 6-O sulfation level in Sdc2 versus Sdc4 heparan sulfate (HS)

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

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

147 cal characteristics, including chain length, sulfation level, and concentration.

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

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

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

151 ries of oligomers with surprisingly distinct sulfation levels.

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

153 ne as an exemplar, we show that the specific sulfation modification of the cell surface and extracell

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

155 igate the effects of amino acid sequence and sulfation modifications on thrombin inhibition and antic

156 S oligosaccharides with distinct lengths and sulfation modifications.

157 eract with the neuroplasticity-relevant CS-E sulfation motif.

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

159 The complex sulfation motifs of heparan sulfate glycosaminoglycans (

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

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

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

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

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

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

166 l processes, with the position and extent of sulfation of a glycoside often playing important roles i

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

168 of longer surviving chains indicate complete sulfation of disaccharides beyond the hexasaccharide cor

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

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

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

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

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

174 3-O-Sulfation of HS is catalyzed by the 3-O-sulfotransferase

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

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

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

178 potential functional importance of N-glycan sulfation of influenza glycoproteins.

179 ence in Sdc4 N-terminal domain increases 6-O sulfation of its HS chains and promotes Sdc2-VEGFA(165)-

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

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

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

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

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

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

186 Tyrosine sulfation of proteins is an important post-translational

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

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

189 orinic acid-catalyzed protocol for selective sulfation of pyranoside derivatives at the equatorial po

190 olecules and revealed that posttranslational sulfation of specific tyrosine residues crucially modula

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

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

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

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

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

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

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

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

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

200 The extent of sulfation of the minimal-length binder (hexamer) is rela

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

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

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

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

205 Blocking sulfation on CD44s modestly decreases the tensile streng

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

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

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

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

210 humans, mutations in the genes encoding the sulfation pathway enzymes underlie a number of developme

211 e review the similarities and differences in sulfation pathways and associated processes in animals a

212 localization, regulation, and importance of sulfation pathways in both kingdoms and the ways in whic

213 , the synthesis of activated sulfate used in sulfation pathways is essential in both animal and plant

214 f different substrates are commonly known as sulfation pathways.

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

216 of other heparan sulfates with regiodefined sulfation pattern for functional study.

217 nces of a given chemokine, the structure and sulfation pattern of a given GAG, and structural differe

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

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

220 The sulfation pattern of the heparan sulfate chains formed d

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

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

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

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

225 des that are highly tunable in structure and sulfation pattern, allowing us to determine how heparana

226 aries with variations in glycan sequence and sulfation pattern.

227 hese interactions often require specific GAG sulfation patterns and involve transmembrane receptors o

228 synthesized HS oligosaccharides with defined sulfation patterns and show that synthetic anticoagulant

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

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

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

232 charides; furthermore, the presence of these sulfation patterns in the plasma of septic patients at i

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

234 Sulfation patterns of CS chains influence their interact

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

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

237 The sulfation patterns of these glycosaminoglycans are highl

238 rmed to confirm glycosaminoglycan levels and sulfation patterns on donor samples (n = 15).

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

240 the existence of core protein-determined HS sulfation patterns that regulate specific biological act

241 es with different chain lengths and N- and O-sulfation patterns via chemical synthesis were systemati

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

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

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

245 n sulfate oligosaccharides with well-defined sulfation patterns.

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

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

248 ctivity questioning the paradigm of how the 'sulfation problem' is handled by the HGM; and 3D crystal

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

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

251 Protein tyrosine O-sulfation (PTS) plays a crucial role in extracellular bi

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

253 aled the catalytic mechanism of the tyrosine sulfation reaction.

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

255 acity for synthesizing activated sulfate for sulfation reactions results in dwarfism, and a complete

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

257 Sulfation recodes the biologic activity of acceptors by

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

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

260 o suppress glycosaminoglycan substitution or sulfation, respectively.

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

262 organosulfates, we developed an alternative sulfation route based on an inexpensive, molecularly eff

263 HS chains is regulated by specific substrate sulfation sequences.

264 x and hybrid N-glycans flanked by a terminal sulfation sequon on Gal-GlcNAc and GalNAc-GlcNAc of sulf

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

266 es and structural data suggest that tyrosine sulfation serves as a receptor mimetic strategy for reco

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

268 Sulfation significantly improved the binding affinity of

269 tool to cell-based studies on the role of a sulfation site in the activation of chemokine receptor C

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

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

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

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

274 ent expression of sulfoproteins with defined sulfation sites in live mammalian cells.

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

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

277 by allowing an unambiguous assignment of the sulfation sites.

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

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

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

281 tructural and energetic determinants of TPST sulfation specificity.

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

283 The versatility of this O-sulfation strategy was demonstrated in the scalable synt

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

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

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

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

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

289 an sulfate fragments (of sufficient size and sulfation to bind BDNF) into the circulation.

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

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

295 Chondroitin disaccharide sulfation was suppressed in all groups with respiratory

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

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

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

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

300 tion, enzymatic epimerization, and enzymatic sulfation with recombinant heparin biosynthetic enzymes