ライフサイエンスコーパス: glycosaminoglycan

1 ifically degrade heparan sulfate, a sulfated glycosaminoglycan.

2 PF4 when it binds to CS, the major platelet glycosaminoglycan.

3 oted by chondroitin sulfate (CS), a sulfated glycosaminoglycan.

4 s, reduced extracellular matrix proteins and glycosaminoglycans.

5 gradient is immobilized via interaction with glycosaminoglycans.

6 hat result from defects in the catabolism of glycosaminoglycans.

7 ediated by either elastin-binding protein or glycosaminoglycans.

8 antity and sulfation patterns of circulating glycosaminoglycans.

9 putative collagen-binding interface aided by glycosaminoglycans.

10 or groups: glycoproteins, proteoglycans, and glycosaminoglycans.

11 sulfoglucosamine residues of heparan sulfate glycosaminoglycans.

12 ially degrade HA and do not cleave any other glycosaminoglycans.

13 hment protein that influences utilization of glycosaminoglycans.

14 lfatases involved in degradation of sulfated glycosaminoglycans.

15 the high-throughput disaccharide analysis of glycosaminoglycans.

16 hat used by endothelial cells to bind FH via glycosaminoglycans.

17 ate the overall structure and activity of HS glycosaminoglycans.

18 tually be used for modification of mammalian glycosaminoglycans.

19 e representatives of two major subclasses of glycosaminoglycans.

20 ously for other sulfated polysaccharides and glycosaminoglycans.

21 cable for labeling and detection of suitable glycosaminoglycans.

22 es high mannose-type N-glycans and decreases glycosaminoglycans.

23 well to cells that are deficient in surface glycosaminoglycans.

24 Hyaluronic acid (HA) is a large glycosaminoglycan abundant in mammalian tissues that has

25 s (VACV) envelope protein D8 is one of three glycosaminoglycan adhesion molecules and binds to the li

26 l bone morphology as well as chondrocyte and glycosaminoglycan amount in adjacent cartilage tissue wh

27 f AF-specific extracellular matrix (sulfated glycosaminoglycan and collagen type I), indicating a fav

28 ociated cartilage matrix alterations such as glycosaminoglycan and fluid contents were found to corre

29 content and orientation, water content, and glycosaminoglycan and/or proteoglycan content both in th

30 It binds glycosaminoglycans and certain phospholipids that can mo

31 ere we show that gG attaches to cell surface glycosaminoglycans and induces lipid raft clustering, in

32 ptide-modified surfaces that can engage both glycosaminoglycans and integrins are effective.

33 engage specific cell-surface ligands (i.e., glycosaminoglycans and integrins), the contribution of s

34 Here, we measured vaspin binding of various glycosaminoglycans and low molecular weight heparins by

35 tracellular matrixes comprise glycoproteins, glycosaminoglycans and proteoglycans that order the envi

36 composed of protein fibrils, hyper-sulphated glycosaminoglycans and serum amyloid P component (SAP).

37 Viral glycan receptors such as glycosaminoglycans and sialic acid-containing carbohydra

38 impairs the binding of CXCL8 to cell surface glycosaminoglycans and the transport of CXCL8 across an

39 d infection of HCT-8 cells were inhibited by glycosaminoglycans and were reduced after heparan sulfat

40 ng, the cartilage was assayed for its water, glycosaminoglycan, and collagen content.

41 e have demonstrated that filoviruses utilize glycosaminoglycans, and more specifically heparan sulfat

42 pid linked and glycans in secretory fluids), glycosaminoglycans, and polysaccharides can be easily la

43 Glycosaminoglycans are a group of negatively charged het

44 Because negatively charged glycosaminoglycans are abundantly present in this layer,

45 Our findings demonstrate that circulating glycosaminoglycans are elevated in patterns characterist

46 The sulfation patterns of these glycosaminoglycans are highly variable, which presents a

47 GAPDH can be secreted outside the cell where glycosaminoglycans are present, it seems plausible that

48 ich applies both in vitro and in vivo, where glycosaminoglycans are strongly associated with amyloid

49 ast, surfaces that interact selectively with glycosaminoglycans are superior to Matrigel in promoting

50 Negatively charged glycosaminoglycans are the major components of the ECM.

51 at heparan sulfate and other closely related glycosaminoglycans are the molecules that are used by fi

52 this study, we determined that cell-surface glycosaminoglycans are utilized by both a vaccine strain

53 e binding of Sema3A to rat brain-derived PNN glycosaminoglycans, as demonstrated by the use of CS-E b

54 as a molecular switch to regulate subsequent glycosaminoglycan assembly.

55 cathepsin K molecule binds to collagen-bound glycosaminoglycans at the gap region and recruits a seco

56 s complicated reactions that turn the simple glycosaminoglycan backbone into highly heterogeneous str

57 is, and the interaction was shown to be with glycosaminoglycans because it was abolished when sulfati

58 roteolysis at a site predicted to generate a glycosaminoglycan-bereft N-terminal fragment, versikine

59 s could potentially be attributed to reduced glycosaminoglycan binding ability, as surface plasmon re

60 giogenic activity of CXCL4L1 by reducing the glycosaminoglycan binding ability.

61 This change leads to a decrease of its glycosaminoglycan binding properties and to an enhanceme

62 , approximately 25 nM) between TSG-6 and the glycosaminoglycan binding site of CXCL8, which antagoniz

63 Structural analyses reveal glycosaminoglycan binding sites on Notum, which probably

64 Cathepsin K dimer and glycosaminoglycan binding sites represent novel targetin

65 ins: the glycoprotein, which plays a role in glycosaminoglycan binding, the fusion (F) protein, which

66 rophin (PTN) is a multifunctional, cationic, glycosaminoglycan-binding cytokine and growth factor inv

67 ing sulfated allosteric modulators (SAMs) of glycosaminoglycan-binding proteins (GBPs), such as human

68 nteraction surface partially overlapping the glycosaminoglycan-binding site.

69 Mutations/polymorphisms within these glycosaminoglycan-binding sites have been associated wit

70 cluding those involved in Golgi trafficking, glycosaminoglycan biosynthesis, and glycosylphosphatidyl

71 (2) GO term "glycosaminoglycan biosynthetic process" was enriched in

72 This glycosaminoglycan blocks the protective effect of Lys-35

73 Furthermore, we demonstrate that these glycosaminoglycans can block entry of and infection by f

74 The resulting accumulation of glycosaminoglycans causes progressive multisystem deteri

75 lyzing the initial and rate-limiting step in glycosaminoglycan chain assembly.

76 this C-terminal heparin-binding domain with glycosaminoglycan chains of proteoglycans at the cell su

77 -OST) family catalyzes rare modifications of glycosaminoglycan chains on heparan sulfate proteoglycan

78 e show that heparan sulfate (HS), a class of glycosaminoglycan chains, regulates the number and asymm

79 h its core protein and with Ptc1 through its glycosaminoglycan chains.

80 Hyaluronan (HA) is a major glycosaminoglycan component of the ECM and plays a signi

81 Hyaluronan is the predominant glycosaminoglycan component of the extracellular matrix

82 om differences in intracellular HA, sulfated glycosaminoglycan concentration, apoptosis, or levels of

83 We observed abnormal glycosaminoglycan concentrations and increased concentra

84 ved from affected individuals and determined glycosaminoglycan concentrations in these cells as well

85 4.7 degrees , T2* was highly correlated with glycosaminoglycan content (r = 0.85, P < .001), the coll

86 was significantly correlated with increasing glycosaminoglycan content for sodium iodide and Gd-DTPA

87 ed cellularity, less vascularity, and higher glycosaminoglycan content when compared with control sam

88 costochondral cells, evidenced by increased glycosaminoglycan content, decreased type I/II collagen

89 vivo human hip cartilage correlates with the glycosaminoglycan content, equilibrium modulus, and coef

90 agen content, and no correlation with DNA or glycosaminoglycan content, indicating there are addition

91 Cellularity and glycosaminoglycans content were significantly higher in

92 Wnt and Hedgehog signal pathways as well as glycosaminoglycan degradation.

93 chondroitinase-ABC concentrations (mimicking glycosaminoglycan depletion) decreased diffusivities and

94 t catabolic stimulation for their effects on glycosaminoglycan deposition as assessed by Alcian blue

95 ds on anabolic gene expression and increased glycosaminoglycan deposition.

96 fractions of the exudate (46.7% increase in glycosaminoglycan deposition; approximately 20% upregula

97 be weakened by charge screening or enzymatic glycosaminoglycan digestion.

98 BIAcore) determined that DMAV binds sulfated glycosaminoglycans (e.g. heparin, KD ~100 nmol/liter), a

99 we show that CD44, a major receptor for the glycosaminoglycan ECM component hyaluronan, coordinates

100 ans (eg, versican, syndecans, biglycan), and glycosaminoglycans (eg, hyaluronan, heparan sulfate) are

101 Sulodexide, a glycosaminoglycan, exerts antithrombotic and profibrinol

102 Herein, we report the first synthesis of a glycosaminoglycan family glycopeptide containing two dif

103 A27 is one of the three glycosaminoglycan (GAG) adhesion molecules and binds to

104 eolysis of the Glu(441)-Ala(442) bond in the glycosaminoglycan (GAG) beta domain of the versican-V1 v

105 In this study, we tested whether glycosaminoglycan (GAG) binding is required for efficien

106 Oligomerization and glycosaminoglycan (GAG) binding of CCL5 and CCL3 are vit

107 en identified a suite of enzymes involved in glycosaminoglycan (GAG) biogenesis and transport, includ

108 Among glycosaminoglycan (GAG) biosynthetic enzymes, the human

109 Among these, the glycosaminoglycan (GAG) chains of proteoglycans shape Hh

110 ored in platelet alpha-granules bound to the glycosaminoglycan (GAG) chains of serglycin.

111 Proteoglycans, a family of glycosaminoglycan (GAG) conjugated proteins, are importa

112 Glycosaminoglycan (GAG) enrichment is a dominant hallmar

113 Heparin and related members of the glycosaminoglycan (GAG) family are highly polyanionic li

114 As members of the glycosaminoglycan (GAG) family, heparin and heparan sulf

115 newly identified xylose kinase essential for glycosaminoglycan (GAG) formation on the protein core of

116 tase involved in the stepwise degradation of glycosaminoglycan (GAG) heparan sulfate.

117 Because matrix glycosaminoglycan (GAG) is known to be important for the

118 r without heparan and/or chondroitin sulfate glycosaminoglycan (GAG) modifications in cells and has e

119 that it is also bound to large interstitial glycosaminoglycan (GAG) networks in different tissues, w

120 Glycosaminoglycan (GAG) polysaccharides have been implic

121 Food grade sulfated glycosaminoglycan (GAG) polysaccharides were successfull

122 des as well as non-protein factors including glycosaminoglycan (GAG) polysaccharides.

123 t combining LIPUS with microbubbles enhanced glycosaminoglycan (GAG) production by 17% (5% with LIPUS

124 Compound 9c was able to inhibit glycosaminoglycan (GAG) release induced by interleukin-1

125 Glycosaminoglycan (GAG) sequences that selectively targe

126 ce sulfatase Sulf1 against its physiological glycosaminoglycan (GAG) target heparan sulfate (HS) by s

127 on production and charge characteristics of glycosaminoglycan (GAG) were examined via metabolic labe

128 Semi-synthetic glycosaminoglycan (GAG), generated from the sulfation of

129 Glycosaminoglycan (GAG)-bound and soluble chemokine grad

130 Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in targe

131 Using wild-type and glycosaminoglycan (GAG)-deficient Chinese hamster ovary

132 ynamic nanomechanical behavior of normal and glycosaminoglycan (GAG)-depleted cartilage, the latter r

133 e the promising therapeutic potential of the glycosaminoglycan (GAG)-like molecule pentosan polysulfa

134 Proteoglycans (PGs), a family of glycosaminoglycan (GAG)-protein glycoconjugates, contrib

135 Degradation of the endothelial glycocalyx, a glycosaminoglycan (GAG)-rich layer lining the vascular l

136 dimers, and mediates its function by binding glycosaminoglycans (GAG) and CXCR2 receptor.

137 an sulfate (HS) and chondroitin sulfate (CS) glycosaminoglycans (GAG) are proteoglycan-associated pol

138 mple synthetic glycans, more complex natural glycosaminoglycans (GAG), and lectins/carbohydrate bindi

139 For the first time, clean CEST contrast for glycosaminoglycans (gagCEST) in cartilage in the human k

140 hment also verified that interaction between glycosaminoglycans (GAGs) and CFH plays an important rol

141 These peptides display high affinity for glycosaminoglycans (GAGs) and compete with functional in

142 his could be mediated by the xyloside-primed glycosaminoglycans (GAGs) and that these differ in compo

143 Glycosaminoglycans (GAGs) are a class of heterogeneous,

144 ractions between chemokines such as CCL5 and glycosaminoglycans (GAGs) are essential for creating hap

145 Glycosaminoglycans (GAGs) are found in intracellular gra

146 Degraded fragments of sulfated glycosaminoglycans (GAGs) are key reporters for profilin

147 Extracellular matrix molecules such as glycosaminoglycans (GAGs) are typical targets for some p

148 Glycosaminoglycans (GAGs) as one major part of the glyco

149 Glycosaminoglycans (GAGs) bind all known amyloid plaques

150 to heparin and brain-derived heparan sulfate glycosaminoglycans (GAGs) but not to the closely related

151 all-beta conformation, which interacts with glycosaminoglycans (GAGs) but not with the specific XCL1

152 ructural characterization of highly sulfated glycosaminoglycans (GAGs) by collisionally activated dis

153 are mediated through the negatively charged glycosaminoglycans (GAGs) chondroitin sulfate and high-m

154 ocyte migration via oligomerization, bind to glycosaminoglycans (GAGs) during the inflammation respon

155 The interaction of chemokines with glycosaminoglycans (GAGs) facilitates the formation of l

156 Glycosaminoglycans (GAGs) govern important functional ch

157 including the accumulation of the undegraded glycosaminoglycans (GAGs) heparan sulfate (HS), and derm

158 Our studies also reveal that R17 binds to glycosaminoglycans (GAGs) in a process dependent upon tw

159 ations leading to inefficient degradation of glycosaminoglycans (GAGs) in lysosomes.

160 of collagen and charged macromolecules like glycosaminoglycans (GAGs) in the interstitial space limi

161 el electrospun scaffold, functionalized with glycosaminoglycans (GAGs) ionically immobilized onto the

162 The ability to interact with cell surface glycosaminoglycans (GAGs) is essential to the cell migra

163 o susceptible host cells by interacting with glycosaminoglycans (GAGs) on the cell surface.

164 chondroitin sulfate/dermatan sulfate (CS/DS) glycosaminoglycans (GAGs) participate in many important

165 Glycosaminoglycans (GAGs) possess considerable heterogen

166 lysine at E2 162 or 247 were more reliant on glycosaminoglycans (GAGs) to enter cells and were select

167 membrane-docking peptide to heparan sulfate glycosaminoglycans (GAGs) with a PTD.

168 nd and lung, we demonstrate that MCK-2 binds glycosaminoglycans (GAGs) with affinities in the followi

169 ize highly sulfated glycans (i.e. mucins and glycosaminoglycans (GAGs)) and to colonize the intestina

170 Glycosaminoglycans (GAGs), a category of linear, anionic

171 research, and this is particularly true for glycosaminoglycans (GAGs), a class of linear sulfated po

172 th the presentation of CXCL8 on cell-surface glycosaminoglycans (GAGs), an interaction that is vital

173 tic activity, which leads to accumulation of glycosaminoglycans (GAGs), and secondary accumulation of

174 Glycosaminoglycans (GAGs), especially heparin and hepara

175 n was demonstrated to interact with sulfated glycosaminoglycans (GAGs), in a Ca(2+)-independent way,

176 e of tissue-specifically expressed, sulfated glycosaminoglycans (GAGs), like HS, in determining FH bi

177 Sema3A interacts with glycosaminoglycans (GAGs), presumably through its C-term

178 te and present CXCL12 via cell-surface-bound glycosaminoglycans (GAGs), thereby attracting CLL cells

179 Furthermore, HS, heparin, and other related glycosaminoglycans (GAGs), to different extents, can bin

180 most complex and important carbohydrates are glycosaminoglycans (GAGs), which display varied stereoch

181 e binding of chemokines to membrane-tethered glycosaminoglycans (GAGs), which establishes a chemokine

182 nant envelope protein of vaccinia virus, for glycosaminoglycans (GAGs)-specific targeting and imaging

183 in the IDUA gene causing the accumulation of glycosaminoglycans (GAGs).

184 ted protein 5/6 (Lrp5/6), Tetraspanin-12 and glycosaminoglycans (GAGs).

185 ), antibodies to PF4 and heparin or cellular glycosaminoglycans (GAGs).

186 the prevention of lysosomal accumulation of glycosaminoglycans (GAGs).

187 factors in the conversion process, including glycosaminoglycans (GAGs).

188 ed charges in cartilage extracellular matrix glycosaminoglycans (GAGs).

189 type II collagen, hyaluronic acid (HA), and glycosaminoglycans (GAGs).

190 highly anionic linear polysaccharides called glycosaminoglycans (GAGs).

191 tain non-proteinaceous components, including glycosaminoglycans (GAGs).

192 e inhibitor (serpin) family are activated by glycosaminoglycans (GAGs).

193 heir envelope glycoproteins and cell-surface glycosaminoglycans (GAGs).

194 matory processes, is known to be affected by glycosaminoglycans (GAGs).

195 t are achieved by interactions with sulfated glycosaminoglycans (GAGs).

196 se is intimately coupled to interaction with glycosaminoglycans (GAGs).

197 oteoglycans are proteins that carry sulfated glycosaminoglycans (GAGs).

198 to be determined whether the interplay among glycosaminoglycans, GAPDH, and alpha-synuclein has a rol

199 lar matrix, consisting of negatively charged glycosaminoglycans, glycoproteins and proteoglycans in t

200 therapeutically significant glycoconjugates (glycosaminoglycans, glycoproteins, glycolipids, glycosyl

201 lasses of glycan including N- and O-glycans, glycosaminoglycans, glycosphingolipids, and glycophospha

202 We found that the type of glycosaminoglycan has a different effect on the kinetics

203 Hyaluronan, a high molecular mass glycosaminoglycan, has been shown by us to be a suitable

204 These complex glycosaminoglycans have important roles in cell adhesion

205 molecular species, such as glycoproteins and glycosaminoglycans, have important biological and therap

206 Cell surface anionic glycosaminoglycans heparan sulfate and HA protect the ce

207 The natural glycosaminoglycan heparin surprisingly inhibited malaria

208 tilization hierarchy indicates that the host glycosaminoglycans heparin (Hep) and heparan sulfate (HS

209 n important constituent of the heterogeneous glycosaminoglycans heparin and heparan sulfate occurring

210 late, bromophenol blue, and resveratrol) and glycosaminoglycans (heparin and heparin disaccharide) di

211 The glycosaminoglycan hyaluronan (HA) accumulates in demyeli

212 king the CD44 transmembrane receptor for the glycosaminoglycan hyaluronan (HA) demonstrate a number o

213 ceptor 4 (TLR4) and the extracellular matrix glycosaminoglycan hyaluronan (HA) on AEC2s are important

214 The high concentration in the stroma of the glycosaminoglycan hyaluronan, together with the large ge

215 ution and includes the high molecular weight glycosaminoglycan, hyaluronan (HA).

216 accompanied by a coordinate loss in another glycosaminoglycan, hyaluronan.

217 For each class of the glycosaminoglycans-hyaluronan (HA), heparan sulfate/hepa

218 We identify the polyanionic glycosaminoglycans hyaluronic acid and heparan sulfate a

219 c acid-a high molecular extracellular matrix glycosaminoglycan implicated in playing an important rol

220 insights into the pathogenic contribution of glycosaminoglycan in SAA1.1-mediated AA amyloid formatio

221 and 30%, respectively, and SDC4 and sulfated glycosaminoglycan in the culture medium were increased b

222 Hyaluronan (HA) is the major glycosaminoglycan in the extracellular matrix.

223 imicking endogenous HA, a large and abundant glycosaminoglycan in the skin.

224 , our study uncovers a novel role of HS-type glycosaminoglycans in a local accumulation of FXIIa on t

225 l-iduronidase activity and clearing elevated glycosaminoglycans in blood and multiple organs.

226 e interaction of Sema3A with CS-E containing glycosaminoglycans in the dense extracellular matrix of

227 unction of glycoproteins, proteoglycans, and glycosaminoglycans in the myocardium may lead to the dev

228 asis is also regulated by negatively charged glycosaminoglycans in the skin interstitium, where sodiu

229 -iduronidase (IDUA), exhibit accumulation of glycosaminoglycans in tissues, with resulting diverse cl

230 on of the endothelial glycocalyx, a layer of glycosaminoglycans (including heparan sulfate, chondroit

231 to probe interactions of AgRP peptides with glycosaminoglycans, including heparan sulfate.

232 T) mass spectrometry to rapidly screen major glycosaminoglycans, including heparin, chondroitin sulfa

233 In a previous work, we showed that glycosaminoglycan-induced GAPDH prefibrillar species acc

234 The structural analysis of these glycosaminoglycans is challenging due to the lability of

235 We also synthesized an orally active glycosaminoglycan (LHbisD4) that specifically binds with

236 glycolic acid (PLGA) microspheres containing glycosaminoglycan-like biopolymers (BPs), was examined.

237 d secretion of lysosomal contents, including glycosaminoglycans, lysosomal hydrolases, and matrix met

238 , the method allows one to clearly demarcate glycosaminoglycan measurements from cartilage and synovi

239 n, indicating that the sulfate groups of the glycosaminoglycan mediate p17 interaction.

240 , G protein coupled receptors, serotonin and glycosaminoglycan metabolisms among others.

241 up of small molecules, called non-saccharide glycosaminoglycan mimetics (NSGMs), as direct allosteric

242 ycles, associated with a significant loss of glycosaminoglycans, mineral content, and ECM-bound cytok

243 Amounts of sulphated glycosaminoglycans, MMPs and TIMPs were assessed using t

244 gical and immunological significance of this glycosaminoglycan modification and for an "ancient glyca

245 a common, but complex, malignancy-associated glycosaminoglycan modification.

246 S cleaved chemokines at the N terminus with glycosaminoglycans modulating cathepsin processing of ch

247 flow applicable for simultaneous analysis of glycosaminoglycans, N-glycans and proteins/peptides from

248 he streptococci can use phage HLs to degrade glycosaminoglycans of the extracellular matrix for sprea

249 ables the long-lived presentation of defined glycosaminoglycans on cell surfaces using HaloTag protei

250 In this study, we investigated the effect of glycosaminoglycans on the kinetics of amyloid fibril for

251 ve a variety of accessory molecules, such as glycosaminoglycans, one of the main components of the ex

252 Heparan sulfate (HS) glycosaminoglycans participate in critical biological pr

253 ec-Fc was specifically inhibited by sulfated glycosaminoglycans, particularly heparin and heparan sul

254 Removal of collagen-associated glycosaminoglycans prevents cathepsin K binding and subs

255 ontent (r = 0.85, P < .001), the collagen-to-glycosaminoglycan ratio (r = -0.79, P < .001), and water

256 dies with differing specificities, including glycosaminoglycan reactivity.

257 hat BTV8H acquired an increased affinity for glycosaminoglycan receptors during passaging in cell cul

258 we show that a genetic point mutation in the glycosaminoglycan recognition motif of Otx2 broadly dela

259 acellular and secreted factor that decreased glycosaminoglycan release and depletion from the cartila

260 cellular matrix production was suppressed as glycosaminoglycan secretion and production of aggrecan,

261 Cartilage sulphated glycosaminoglycan (sGAG) and collagen content were asses

262 Digesting glycosaminoglycan side chains of CSPG with chondroitinas

263 glycin proteoglycans with negatively charged glycosaminoglycan side chains of either heparin or chond

264 se that specifically degrades the unbranched glycosaminoglycan side chains of HSPGs.

265 animals not only demonstrated reductions in glycosaminoglycan storage in most tissues, but most also

266 creased in visceral organs of MPS-I animals, glycosaminoglycans storage was reduced, and skeletal phe

267 eta-d-xylopyranoside or chlorate to suppress glycosaminoglycan substitution or sulfation, respectivel

268 bsent, as occurred when all three N-terminal glycosaminoglycan substitution sites were mutated to ala

269 ulfate groups of sulfated GalNAc residues of glycosaminoglycans such as chondroitin and dermatan sulf

270 VACV has been shown to utilize cell surface glycosaminoglycans such as heparan sulfate (HS), the ext

271 ry TGFbeta1 and osteogenic BMP-2, as well as glycosaminoglycans such as heparan sulfate and chondroit

272 binding is shown to be selective over other glycosaminoglycans, such as hyaluronic acid and chondroi

273 mes specifically hydrolyze sulfate esters in glycosaminoglycans, sulfolipids, or steroid sulfates, th

274 ow that biallelic mutations in EXTL3 disturb glycosaminoglycan synthesis and thus lead to a recogniza

275 gar donors were then tested as substrates in glycosaminoglycan synthesis catalyzed by various synthas

276 aran sulfate and following the inhibition of glycosaminoglycan synthesis or sulfation in HCT-8 cells.

277 ter heparan sulfate removal or inhibition of glycosaminoglycan synthesis or sulfation.

278 NOX4) and pathways (such as proteoglycan and glycosaminoglycan synthesis) involved in growth.

279 y decreased in CHO cell mutants defective in glycosaminoglycan synthesis.

280 A/K45A retained higher affinity for sulfated glycosaminoglycans than K42A/K110A and exhibited increas

281 Hyaluronan (HA) is an extracellular matrix glycosaminoglycan that is present in pancreatic islets,

282 Heparin is a highly sulfated glycosaminoglycan that shares a common biosynthetic path

283 abolism has been linked to the metabolism of glycosaminoglycans that are exposed on injured heart val

284 g specificity for substructures within these glycosaminoglycans that display a different degree of su

285 tructure, also enhancing the binding of this glycosaminoglycan to its cell surface receptor, CD44.

286 d thus extend the ancestry of this important glycosaminoglycan to the premetazoan era.

287 in human cells and found that RVFV utilizes glycosaminoglycans to attach to host cells.

288 rate that FXIIa utilizes cell membrane-bound glycosaminoglycans to interact with the cell surface of

289 f murine interferon gamma (IFN-gamma), binds glycosaminoglycans to modulate serum and interstitial cy

290 ad ECs (RFPECs), including proteoglycans and glycosaminoglycans, to observe how each component indivi

291 h specific sulfated chondroitin sulfate (CS) glycosaminoglycans using chemically modified liposomes.

292 In addition to influencing glycosaminoglycan utilization, we identified roles for t

293 s and with the host cell-surface receptor(s)/glycosaminoglycans via its N-terminal collagen-like stal

294 des that can be used to differentiate parent glycosaminoglycans via unsupervised multivariate analysi

295 face, which colocalized with CXCL8, and this glycosaminoglycan was 2,6-O- and 3-O-sulfated.

296 e polyanions include heparan sulfate (HS), a glycosaminoglycan with a highly diverse range of structu

297 e data enabled facile differentiation of the glycosaminoglycans with high throughput.

298 of enzymes that target substructures of the glycosaminoglycans with variable sulfation or that the g

299 Highly sulfated glycosaminoglycans within the cartilage matrix provide s

300 skin interstitium, where sodium is bound to glycosaminoglycans without commensurate effects on extra