ライフサイエンスコーパス: GAG

1 GAG-protein interactions participate in neuronal develop

2 GAGs affect the kinetics and pathway of Abeta self-assem

3 GAGs are highly negatively charged polysaccharides and i

4 GAGs are ubiquitous constituents of connective tissue, c

5 GAGs induce fast sCT fibrillation at acidic pH and only

6 lthough no co-crystal structure of the IL-10.GAG complex could be obtained, its structural characteri

7 t experimental characterization of the IL-10.GAG complex structure and provides the starting point fo

8 articular, experimental evidence about IL-10/GAG binding sites is lacking, despite its importance for

9 The molecular mechanism of the IL-10/GAG interaction is unclear.

10 of a 7-base pair response element, either 5- GAG CA-3 or 5- GAG CA-3 (where M = 5-methylcytosine).

11 Zta-response elements, including meZRE1 (5- GAG C A-3) and meZRE2 (5- GAG G A-3), where a methylated

12 cluding meZRE1 (5- GAG C A-3) and meZRE2 (5- GAG G A-3), where a methylated cytosine occupies one of

13 r response element, either 5- GAG CA-3 or 5- GAG CA-3 (where M = 5-methylcytosine).

14 along with other residues combine to form a GAG-binding groove in the CCL3 oligomer.

15 y slip bond interaction can be observed in a GAG system where this site is explicitly lacking.

16 e report the experimental determination of a GAG binding site of IL-10.

17 to distinct patches on Norrin, and reveal a GAG binding site spanning Norrin and Fz4CRD.

18 e receptor-binding domain, indicating that a GAG-bound chemokine cannot activate the receptor.

19 ith molecular dynamics simulations yielded a GAG binding model.

20 such as 1B6 that recognize the more abundant GAG-bound form of the chemokine may not be the optimal s

21 of defects including reduced XylT activity, GAG incorporation of (35)SO4, and heparan sulfate proteo

22 rties and dimer-dimer interactions to affect GAG binding and oligomerization.

23 ndicated that the dimer is the high-affinity GAG binding ligand and that lysine residues from the N-l

24 CR2 agonists, the dimer is the high-affinity GAG ligand, lysine and arginine residues located in two

25 indicate that the dimer is the high-affinity GAG ligand.

26 that the catch bond character of HD against GAGs could be attributed to the GAG 6-O-sulfation site w

27 We have analyzed GAGs in C. elegans using reversed-phase ion-pairing HPLC

28 nfidence interval: 0.609, 0.976) for APT and GAG, respectively.

29 ant protein (gCDeltamuc) in cell culture and GAG-binding assays, respectively.

30 Changes in sodium MR imaging and GAG CEST in men may reflect a decrease of GAG content in

31 Further, binding interactions and GAG geometry in CXCL5 are novel and distinctly different

32 Such complexity in oligomerization and GAG binding enables intricate, physiologically relevant

33 ich are versatile for controlled protein and GAG immobilization, can be effectively used as molecular

34 Results obtained for normal and GAGs-deficient cells showed that the recombinant protein

35 ally relevant interaction between Sema3A and GAGs, thus revealing SICHI as a new, to our knowledge, c

36 ainst both purified and cell wall-associated GAG.

37 consistent with close (<5 A) contact between GAG anomeric position(s) and one or more histidine resid

38 ions, and there is extensive overlap between GAG and receptor-binding domains.

39 que non-chemokine domain, both of which bind GAGs and are critical for GAG-dependent oligomerization

40 mutant of a residue that is involved in both GAG binding and receptor signaling showed the highest re

41 ent, providing compelling evidence that both GAG-binding domains mediate in vivo trafficking.

42 We found that these peptides bind to both GAGs with affinities in the low-micromolar range.

43 ccurately the binding poses of protein-bound GAGs.

44 ical shift perturbations of IL-10 induced by GAG binding were used to narrow down the location of the

45 e, histidine (His-23) may contribute to CCL5-GAG interactions when the pH drops just below neutral, a

46 g sites on chemokines overlap with chemokine GAG-binding sites, and that the affinities of Link_TSG6

47 Chemokine-GAG interactions are crucial to facilitate chemokine imm

48 es 1-85 nm) broadly correlate with chemokine-GAG affinities.

49 mmation based on interference with chemokine-GAG interactions.

50 ulator of chemokines by modulating chemokine/GAG interactions, which may be a major mechanism by whic

51 n in both the relative proteoglycan content (GAG/CH3) (p = 0.08) and collagen maturity (p = 0.57).

52 evelopment of bioactive compounds to correct GAG synthesis disorders implicated in different types of

53 sis or molecular mechanisms underlying CXCL5-GAG interactions.

54 s spectrometry on urine samples to determine GAG (heparan sulfate, chondroitin sulfate, and hyaluroni

55 ite and to assess the affinity for different GAG molecules.

56 t time, opposing functions for the different GAG modifications on TbetaRIII suggesting that Wnt inter

57 intake and neurohumoral alterations disrupt GAG structure, leading to loss of the interstitial buffe

58 that these chemokine oligomers have distinct GAG-binding mechanisms.

59 nly these two GAG chains, but not downstream GAG attachment sites, was cleaved efficiently.

60 Moreover, a diminished endothelial GAG network (the endothelial glycocalyx) results in incr

61 g a positive feedback loop to further enrich GAG content and promote disease progression.

62 geted cells as well as to isolate and enrich GAGs-associated proteins on cell membrane.

63 The enhanced iron uptake through enzymatic GAG depolymerisation could be due to the combined effect

64 An exonic GAG-repeat motif in these IR regions may function as a r

65 hese residues are also involved in extensive GAG interactions.

66 ompete with functional intact chemokines for GAG binding, the longest peptide (CXCL9(74-103)) being t

67 both of which bind GAGs and are critical for GAG-dependent oligomerization of the full-length protein

68 Sph3 is a glycoside hydrolase essential for GAG production and defines a new glycoside hydrolase fam

69 other members of the Bunyaviridae family for GAG-dependent infection suggested that the interaction w

70 ymatic oligosaccharide synthesis methods for GAG-derived motifs, rational and high-throughput design

71 demonstrated that the gene is necessary for GAG production.

72 proposed to encode the proteins required for GAG biosynthesis.

73 Both domains were required for GAG-dependent oligomerization of full-length MCK-2.

74 al and high-throughput design strategies for GAG-based materials, and the utilization of the factor-s

75 CDeltamuc exhibited a decreased affinity for GAGs and a slower dissociation, indicating that once for

76 kine-derived peptides with high affinity for GAGs may be used as anti-inflammatory peptides; by compe

77 ng in the proposal of a new binding site for GAGs.

78 and the biochemical characterization of four GAG-specific sulfatases.

79 The exopolysaccharide galactosaminogalactan (GAG) contributes to the virulence of A. fumigatus.

80 indicating that once formed, the gCDeltamuc-GAG complex is more stable.

81 We showed that this GET (GAG-binding enhanced transduction) system could deliver

82 Glycosaminoglycan (GAG) enrichment is a dominant hallmark of early CAVD, bu

83 Glycosaminoglycan (GAG) polysaccharides have been implicated in a variety o

84 Glycosaminoglycan (GAG) sequences that selectively target heparin cofactor

85 endothelial glycocalyx, a glycosaminoglycan (GAG)-rich layer lining the vascular lumen, is associated

86 Among glycosaminoglycan (GAG) biosynthetic enzymes, the human beta1,4-galactosylt

87 Oligomerization and glycosaminoglycan (GAG) binding of CCL5 and CCL3 are vital for the function

88 ith microbubbles enhanced glycosaminoglycan (GAG) production by 17% (5% with LIPUS alone), and type I

89 lose kinase essential for glycosaminoglycan (GAG) formation on the protein core of proteoglycans, fro

90 te of enzymes involved in glycosaminoglycan (GAG) biogenesis and transport, including several compone

91 protein factors including glycosaminoglycan (GAG) polysaccharides.

92 und to large interstitial glycosaminoglycan (GAG) networks in different tissues, which have an import

93 lycans (PGs), a family of glycosaminoglycan (GAG)-protein glycoconjugates, contribute to animal physi

94 against its physiological glycosaminoglycan (GAG) target heparan sulfate (HS) by single molecule forc

95 Moreover, 1B6 recognized glycosaminoglycan (GAG)-bound CXCL10, resulting in target-mediated clearanc

96 nd/or chondroitin sulfate glycosaminoglycan (GAG) modifications in cells and has established roles in

97 Food grade sulfated glycosaminoglycan (GAG) polysaccharides were successfully extracted from ch

98 Semi-synthetic glycosaminoglycan (GAG), generated from the sulfation of hyaluronic acid, a

99 pha-granules bound to the glycosaminoglycan (GAG) chains of serglycin.

100 nd related members of the glycosaminoglycan (GAG) family are highly polyanionic linear saccharides th

101 rapeutic potential of the glycosaminoglycan (GAG)-like molecule pentosan polysulfate (PPS) to allevia

102 A27 is one of the three glycosaminoglycan (GAG) adhesion molecules and binds to heparan sulfate.

103 its function by binding glycosaminoglycans (GAG) and CXCR2 receptor.

104 ns, more complex natural glycosaminoglycans (GAG), and lectins/carbohydrate binding proteins using ma

105 Glycosaminoglycans (GAGs) are a class of heterogeneous, often highly sulfate

106 Glycosaminoglycans (GAGs) as one major part of the glycocalyx are involved i

107 Glycosaminoglycans (GAGs) bind all known amyloid plaques and help store prot

108 Glycosaminoglycans (GAGs) govern important functional characteristics of the

109 Glycosaminoglycans (GAGs), a category of linear, anionic polysaccharides, ar

110 Glycosaminoglycans (GAGs), especially heparin and heparan sulfate (HS), modu

111 mokines such as CCL5 and glycosaminoglycans (GAGs) are essential for creating haptotactic gradients t

112 5/6), Tetraspanin-12 and glycosaminoglycans (GAGs).

113 ortant carbohydrates are glycosaminoglycans (GAGs), which display varied stereochemistry, chain lengt

114 nstrate that MCK-2 binds glycosaminoglycans (GAGs) with affinities in the following order: heparin >

115 2 via cell-surface-bound glycosaminoglycans (GAGs), thereby attracting CLL cells and protecting them

116 known to be affected by glycosaminoglycans (GAGs).

117 family are activated by glycosaminoglycans (GAGs).

118 and heparin or cellular glycosaminoglycans (GAGs).

119 h the negatively charged glycosaminoglycans (GAGs) chondroitin sulfate and high-molecular-weight hyal

120 isplay high affinity for glycosaminoglycans (GAGs) and compete with functional intact chemokines for

121 n of vaccinia virus, for glycosaminoglycans (GAGs)-specific targeting and imaging of living cells.

122 us components, including glycosaminoglycans (GAGs).

123 leads to accumulation of glycosaminoglycans (GAGs), and secondary accumulation of gangliosides.

124 sing the accumulation of glycosaminoglycans (GAGs).

125 ysosomal accumulation of glycosaminoglycans (GAGs).

126 247 were more reliant on glycosaminoglycans (GAGs) to enter cells and were selected for by passage in

127 d by the xyloside-primed glycosaminoglycans (GAGs) and that these differ in composition depending on

128 parin, and other related glycosaminoglycans (GAGs), to different extents, can bind to and block GP-me

129 -derived heparan sulfate glycosaminoglycans (GAGs) but not to the closely related chondroitin sulfate

130 ptide to heparan sulfate glycosaminoglycans (GAGs) with a PTD.

131 o interact with sulfated glycosaminoglycans (GAGs), in a Ca(2+)-independent way, resulting in the pro

132 ally expressed, sulfated glycosaminoglycans (GAGs), like HS, in determining FH binding to and activit

133 teractions with sulfated glycosaminoglycans (GAGs).

134 eins that carry sulfated glycosaminoglycans (GAGs).

135 of CXCL8 on cell-surface glycosaminoglycans (GAGs), an interaction that is vital for the function of

136 roteins and cell-surface glycosaminoglycans (GAGs).

137 lation of the undegraded glycosaminoglycans (GAGs) heparan sulfate (HS), and dermatan sulfate (DS), p

138 on, which interacts with glycosaminoglycans (GAGs) but not with the specific XCL1 receptor, XCR1.

139 ells by interacting with glycosaminoglycans (GAGs) on the cell surface.

140 Sema3A interacts with glycosaminoglycans (GAGs), presumably through its C-terminal basic region.

141 pled to interaction with glycosaminoglycans (GAGs).

142 etics and mobility studies using end-grafted GAG chains that mimic the end attachment of these chains

143 We conclude that hCXCL1-GAG interactions provide stringent control over regulati

144 rding the structural basis underlying hCXCL1-GAG interactions.

145 However, it remains unclear how GAG structures are changed during the aging process.

146 ermine the possible mechanism explaining how GAGs promote iron uptake by the Caco-2 cells.

147 e, new insights into the dynamics of the HSV-GAG interaction.

148 in modulating the characteristics of the HSV-GAG interaction.

149 h the multivalent binding to the immobilized GAG brushes ensures firm virus attachment to the interfa

150 ce platform consisting of end-on immobilized GAGs.

151 r than the Km value and efficiently impaired GAG synthesis in a cell assay.

152 s of the chemokine domain that are important GAG binding determinants.

153 Differences in GAG binding to fibrils with distinct sequence and/or str

154 y charged and fully exposed motif, KKWVR, in GAG binding.

155 of the invariant arginine anchor residue in GAG result in global redistribution of PFV and macaque s

156 To determine the role of Sph3 in GAG biosynthesis, we determined the structure of Aspergi

157 Increasing GAG sulfation expands the pH range for binding.

158 a-domain binding, indicating two independent GAG-binding sites.

159 ngs suggesting distinct roles for individual GAGs in outcomes related to valve lesion progression, as

160 on mechanism of sugar analogs for inhibiting GAG/glycan biosynthesis.

161 s have been proven to stabilize interstitial GAG networks.

162 activated form, it was not incorporated into GAGs.

163 Here we investigate GAG interactions with the peptide hormone salmon calcito

164 unctionalizations of synthesized or isolated GAGs are considered.

165 The mean GAG CEST value in the whole tendon was parallel to the s

166 cated in two non-overlapping domains mediate GAG interactions, and there is extensive overlap between

167 able to study how monovalent and multivalent GAG.protein bonds respond to directed mechanical forces.

168 spatial arrangement of sulfates along native GAG chains may play a role in modulating the characteris

169 ey role in HSV binding, we tested two native GAGs (chondroitin sulfate and heparan sulfate) and compa

170 Diffusion was faster on the two native GAGs, one of which, chondroitin sulfate, was also charac

171 ithin 30min and enhanced the accumulation of GAG in the rectum compared to traditional enema-based de

172 tic measurements, and in cellulo analysis of GAG anabolism and decorin glycosylation, we mapped the o

173 of the potential therapeutic application of GAG polymers, fragments, and also derivatives toward dif

174 ressed this by characterizing the binding of GAG heparin oligosaccharides to hCXCL1 using NMR spectro

175 nd GAG CEST in men may reflect a decrease of GAG content in the Achilles tendon after ciprofloxacin i

176 possible due to the extremely high degree of GAG heterogeneity.

177 Matrix-mediated delivery of GAG by SELP represents an innovative method for more eff

178 To enhance the delivery of GAG, we created an in situ gelling rectal delivery syste

179 Depolymerisation of GAG polysaccharides to oligosaccharides further improved

180 report the first high-resolution details of GAG-Abeta fibril interactions from the perspective of th

181 he prophylactic delivery of a single dose of GAG from a SELP matrix administered prior to irradiation

182 rmore we observed that a notable fraction of GAG-bound virions exhibit lateral mobility, although the

183 nical forces in the assembly and function of GAG-rich extracellular matrices.

184 ial sulfatases allowed the identification of GAG-specific sulfatases selective for the type of saccha

185 In septic shock, indices of GAG fragmentation correlated with both the development o

186 es a valuable probe for the investigation of GAG biology and opens avenues toward the development of

187 le method for analyzing the nanomechanics of GAG.protein interactions at the level of single GAG chai

188 However, the nature of GAG binding to vaspin is not known.

189 petition experiments indicated an overlap of GAG and chemokine receptor CCR2 binding sites.

190 strict Ty1 mobility whereas other regions of GAG inhibit mobility weakly if at all.

191 target for the development of regulators of GAG synthesis in therapeutics.

192 Our structures of GAG-bound CCL5 and CCL3 oligomers reveal that these chem

193 ng and therefore masking the availability of GAGs.

194 uM 6F-GalNAc (Ac3) inhibited biosynthesis of GAGs (chondroitin/dermatan sulfate by approximately 50-6

195 of the factor-scavenging characteristics of GAGs are highlighted.

196 OxLDL also increased VIC deposition of GAGs, thereby creating a positive feedback loop to furth

197 igned surfaces that afford immobilization of GAGs and receptors at controlled nanoscale organizations

198 Incorporation of GAGs into biomaterials opens up new routes for the prese

199 n understanding and interpreting the role of GAGs in neural development and axonal regeneration after

200 arizes the progress of chemical syntheses of GAGs over the last 10 years.

201 ng unable to recognize CXCL10 immobilized on GAG, we observed a similar superior control of diabetes

202 chemokines for binding and immobilization on GAGs, these peptides may lower chemokine presentation on

203 Conversely, other GAGs did not demonstrate significant binding, nor did th

204 differentially mediated by HS but not other GAGs.

205 cterized by the highest association rate per GAG chain.

206 tudy we isolated XylNapOH- and XylNap-primed GAGs from a breast carcinoma cell line, HCC70, and a bre

207 mposition of the XylNapOH- and XylNap-primed GAGs, which differed between the two cell lines but was

208 y preventing accumulation of proinflammatory GAGs within inflamed joint tissue, a trait that may be s

209 ototype foamy virus (PFV) structural protein GAG associates with chromosomes via a chromatin-binding

210 ction of CXCL10 with GAGs, did not recognize GAG-bound CXCL10, and did not display target-mediated dr

211 hat the geranylated tRNA(Glu) UUC recognizes GAG more efficiently than GAA.

212 Mutants from both domains showed reduced GAG heparin binding affinities and reduced neutrophil re

213 genistein-modulated gene network regulating GAG biosynthesis and degradation, taking into considerat

214 t majority of studies of heparin (or related GAGs) interactions with its client proteins use syntheti

215 s strongly suggest that HS and other related GAGs are attachment receptors that are utilized by filov

216 thogenic and attenuated RVFV strains require GAGs for efficient infection on some, but not all, cell

217 ge degradation treatment with F4 inhibited s-GAG release from IL-1beta-treated human cartilage explan

218 binds to GAGs, thereby perturbing the Sema3A-GAG interaction.

219 Soluble heparinase-sensitive GAGs from Idua(-/-) BM and specifically 2-O-sulfated HS,

220 rlecan heparan sulfate chains than serglycin GAG chains.

221 arger number of gCDeltamuc bound to a single GAG chain, compared with native gC.

222 .protein interactions at the level of single GAG chains, which provides new molecular-level insight i

223 Although some GAG-specific bacterial sulfatase activities have been de

224 questration, whereas the chondroitin sulfate GAG chains on TbetaRIII promote Wnt3a signaling.

225 t to the closely related chondroitin sulfate GAGs.

226 -primed chondroitin sulfate/dermatan sulfate GAGs derived from HCC70 cells had a cytotoxic effect on

227 manner by the XylNap-primed heparan sulfate GAGs.

228 s research establishes that chicken sulfated GAG polysaccharides can enhance iron uptake by Caco-2 ce

229 Heparin, the most highly sulfated GAG, binds sCT in the pH interval 3-7.

230 ling Wnt3a availability through its sulfated GAG chains.

231 Both the cartilage and skin sulfated GAG polysaccharides showed greater ferritin formation co

232 The sulfated GAG oligosaccharides derived from cartilage possessed th

233 ve charge, and its interaction with sulfated GAG-polymers were quantitatively investigated using atom

234 HSV-1 recognized all sulfated GAGs, but not the nonsulfated hyaluronan, indicating tha

235 While no sulfated GAGs have been found in marine sponges, chondroitin sulf

236 sive, colorimetric urinary assay of sulfated GAGs.

237 ue GAG sequences that can selectively target GAG-binding protein(s), which may lead to chemical biolo

238 ted a similar requirement for the N-terminal GAG chains and Glu(441).

239 d CCL2 are non-redundant chemokines and that GAG chain density may provide a mechanism for regulating

240 We conclude that GAG interactions and receptor activity of CXCL1 monomers

241 omponent of AD plaques, and they reveal that GAG-amyloid interactions display a range of affinities t

242 Our results showed that GAG model compounds, a pentasaccharide (fondaparinux, FX

243 We validate that GAG-Dock reproduces accurately (<1-A rmsd) the crystal s

244 the arrangement of sulfate groups along the GAG chain, plays a key role in HSV binding, we tested tw

245 normalized sodium MR imaging signal and the GAG CEST effect in the Achilles tendon of healthy volunt

246 with the variable echo-time sequence and the GAG CEST values were acquired with a three-dimensional r

247 ) has also been identified previously as the GAG-binding domain for the related chemokine CXCL8/IL-8.

248 lude that a finely tuned balance between the GAG-bound dimer and free soluble monomer regulates CXCL5

249 ing, but distinct from those involved in the GAG-binding function of XCL1.

250 ontains a mucin-like region located near the GAG-binding site, which may affect the binding activity.

251 magic-angle spinning solid-state NMR of the GAG bound to 3Q fibrils, and measurements of dynamics re

252 y the method to study the interaction of the GAG polymer hyaluronan (HA) with CD44, its receptor in v

253 ating selectivity in the interactions of the GAG with the fibril that extends beyond general electros

254 Solid-state NMR analysis of the GAG-3Q fibril complex revealed an interaction site at th

255 SV-1 gC is involved in the modulation of the GAG-binding activity, a feature of importance both for u

256 e here the development and validation of the GAG-Dock computational method to predict accurately the

257 mplementarity of the sulfate moieties on the GAG and charged residues displayed on the fibril surface

258 Based on the GAG binding data, an anti-inflammatory role for CXCL9(74

259 lycoproteins and sulfated saccharides on the GAG chain.

260 owledge, class of inhibitors that target the GAG-protein interaction.

261 We have shown previously that the GAG low-molecular-weight heparin (LMWH) binds to Abeta40

262 Binding analysis indicated that the GAG proxy heparin has a remarkably high affinity for Abe

263 ithin a monomer and, interestingly, that the GAG-binding domain overlaps with the receptor-binding do

264 We also show that the GAG-bound hCXCL1 completely occlude receptor binding.

265 f HD against GAGs could be attributed to the GAG 6-O-sulfation site whereas only slip bond interactio

266 MAbs was mapped to a region adjacent to the GAG binding site, a finding which suggests that group I

267 g-17 and -47 in CCL5, which overlap with the GAG-binding (44)RKNR(47) "BBXB" motifs.

268 leukocytes into inflammatory sites, and the GAGs that interact with CCL5 with the highest affinity a

269 ant protein rDA27(aa 33-84) that removes the GAGs-binding sequences was also used for comparison.

270 the two cell lines but was similar when the GAGs were derived from the same cell line.

271 that the recombinant proteins maintain their GAG-targeting activities even after immobilization on th

272 dermatan sulfate and that PF4 binds to these GAG chains.

273 These GAGs may have therapeutic potential in treating EBOV- an

274 Both MCK-2 domains bound these GAGs independently, and computational analysis together

275 n orchestrates leukocyte recruitment through GAG binding and G protein-coupled receptor activation.

276 d, possibly through contacts to Lys(18) Thus GAGs significantly modulate sCT fibrillation in a pH-dep

277 Recent approaches to GAG-based materials are reviewed, highlighting the forma

278 f is key for the binding of CC chemokines to GAG.

279 native HSV-1 (i.e. decreased sensitivity to GAG-based inhibitors of virus attachment to cells and re

280 Thus, binding to GAGs in the extracellular matrix can direct and regulate

281 ses with the greatest reliance on binding to GAGs replicated to higher titers in the brain and more e

282 the E2 glycoprotein, mediated by binding to GAGs, determine selective advantage and plaque size in B

283 rminus-derived basic peptides for binding to GAGs.

284 techniques, we observed that SICHI binds to GAGs and competes with Sema3A C-terminus-derived basic p

285 ypothesis, according to which SICHI binds to GAGs, thereby perturbing the Sema3A-GAG interaction.

286 of these viral protein-FND conjugates toward GAGs binding was examined by flow cytometry, fluorescenc

287 A construct including only these two GAG chains, but not downstream GAG attachment sites, was

288 l techniques can lead to discovery of unique GAG sequences that can selectively target GAG-binding pr

289 Early indices of urinary GAG fragmentation predict acute kidney injury and in-hos

290 ghlights the complexity of multivalent virus-GAG interactions and suggests that the spatial arrangeme

291 e oligomerized; thus, the mechanism by which GAG binds these chemokine oligomers has been elusive.

292 Therefore, we investigated which GAGs mediate human FH and recombinant human FH complemen

293 domain (Fz4CRD), of this complex bound with GAG analogues, and of unliganded Norrin and Fz4CRD.

294 analogs for their capacity to interfere with GAG biosynthesis.

295 1 lysine-substituted elastin-like unit) with GAG GM-0111, we created an injectable delivery platform

296 ignificance of the interaction of IL-10 with GAGs.

297 F11 inhibited the interaction of CXCL10 with GAGs, did not recognize GAG-bound CXCL10, and did not di

298 nfection suggested that the interaction with GAGs is not universal among bunyaviruses, indicating tha

299 data suggest that CHIKV E2 interactions with GAGs diminish dissemination to lymphoid tissue, establis

300 sCT fibrillates without GAGs, but heparin binding accelerates the process by dec