ライフサイエンスコーパス: GAG

1 GAG is a heterogeneous linear alpha-1,4-linked exopolysa

2 GAG-DMMB and GAG-MS (g/mol creatinine) were increased in

3 GAG-protein interactions participate in neuronal develop

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

5 GAGs were selectively removed from demineralized mouse p

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

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

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

9 n both MSM (r = 0.48, GAG-DMMB and r = 0.43, GAG-MS; P < 0.001) and SM patients (r = 0.47, P = 0.002

10 with parasite biomass in both MSM (r = 0.48, GAG-DMMB and r = 0.43, GAG-MS; P < 0.001) and SM patient

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

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

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

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

15 concentration in healthy and arthritic (50% GAG depleted) cartilage, respectively.

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

17 could be restored by addition of heparin, a GAG similar to heparan sulfate.

18 In mice, a GAG-deficient Aspergillus mutant (Deltagt4c) did not eli

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

20 ith molecular dynamics simulations yielded a GAG binding model.

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

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

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

24 given GAG, and structural differences among GAGs and among chemokines impact binding interactions.

25 lastic lamellae, lost SMC contractility, and GAG production within an intra-lamellar space, focusing

26 GAG-DMMB and GAG-MS (g/mol creatinine) were increased in SM (mean, 95

27 In SM patients, GAG-DMMB and GAG-MS were increased in those with a fatal outcome (n =

28 er proportion of cytokine-producing ENV- and GAG-specific CD4 and CD8 T cells compared with LT.

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

30 rtilage had generally the highest moduli and GAG depleted samples the lowest.

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

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

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

34 The N-lobe of Arc GAG domain acquired a hydrophobic binding pocket in high

35 and amygdala-dependent learning requires Arc GAG domain phosphorylation.

36 Here, we report that Arc GAG also acquired phosphorylation sites that can acutely

37 CaMKII phosphorylates the N-lobe of the Arc GAG domain and disrupts an interaction surface essential

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

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

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

41 , a readily available, promiscuously-binding GAG.

42 d discovered that CHIKV preferentially binds GAGs.

43 minoglycans) using a dimethylmethylene blue (GAG-DMMB) and liquid chromatography-tandem mass spectrom

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

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

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

47 ccurately the binding poses of protein-bound GAGs.

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

49 Chemokine-GAG interactions are crucial to facilitate chemokine imm

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

51 or AKT, differentially influenced collagen, GAG and elastin in a tissue-dependent manner.

52 We hypothesized that inhibiting CS-GAG signaling in the TME would stem GBM invasion.

53 ite of CS-A and CS-E [4- and 4,6-sulfated CS-GAG (COMP)] matrices compared with monosulfated (4-sulfa

54 sis or molecular mechanisms underlying CXCL5-GAG interactions.

55 Here, we show that Agd3 deacetylates GAG in a metal-dependent manner, and is the founding mem

56 specific IgG or IgE in plasma, (d) decreased GAG storage in liver, and (e) fewer circulating immune c

57 Pel polysaccharide biosynthesis, can degrade GAG, disrupt A. fumigatus biofilms, and attenuate fungal

58 similarities given their ability to degrade GAG and disrupt A. fumigatus biofilms.

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

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

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

62 , which is likely influenced by differential GAG receptor binding specificities.

63 ce GAGs and genetic ablation that diminishes GAG expression reduced CHIKV binding and infectivity of

64 an active glycoside hydrolase that disrupts GAG-dependent A. fumigatus and Pel polysaccharide-depend

65 DMMB-GAG and mass spectrometry (MS)-GAG (g/mol creatinine) we

66 In CM survivors, urinary GCX DMMB-GAG normalized by d 3.

67 HCs (P < 0.001), with no differences in DMMB-GAG and MS-GAG between CM and UM children or between tho

68 After adjusting for disease severity, DMMB-GAG was significantly associated with parasitemia [parti

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

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

71 Proteomic analysis confirmed that enzymatic GAG removal does not significantly alter protein content

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

73 Here, we report the first GAG polysaccharide-based photoaffinity probes for the sy

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

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

76 iated with low-energy activation methods for GAGs and other sulfated oligosaccharides.

77 as been shown to be safe, preventing further GAG loss and cytotoxicity.

78 Galactosaminogalactan (GAG) is an integral component of the A. fumigatus biofil

79 The exopolysaccharide galactosaminogalactan (GAG) is an important virulence factor of the fungal path

80 the biofilm matrix is galactosaminogalactan (GAG), a cationic polymer of alpha-1,4-linked galactose a

81 at the polysaccharide galactosaminogalactan (GAG) of A. fumigatus is a PAMP that activates the NLRP3

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

83 e structure and sulfation pattern of a given GAG, and structural differences among GAGs and among che

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

85 Glycosaminoglycan (GAG) sequences that selectively target heparin cofactor

86 Glycosaminoglycan (GAG)-protein interactions mediate critical physiological

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

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

89 protein factors including glycosaminoglycan (GAG) polysaccharides.

90 ing evidence of increased glycosaminoglycan (GAG) content in patients with post-stroke muscle stiffne

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

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

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

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

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

96 en shown extensively that glycosaminoglycan (GAG)-protein interactions can induce, accelerate, and im

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

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

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

100 Glycosaminoglycans (GAG) are important regulators of angiogenic processes.

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

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

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

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

105 Glycosaminoglycans (GAGs) govern important functional characteristics of the

106 Glycosaminoglycans (GAGs) play vital roles in many biological processes and

107 Glycosaminoglycans (GAGs) represent a promising class of bio-derived materia

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

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

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

111 family are activated by glycosaminoglycans (GAGs).

112 known to be affected by glycosaminoglycans (GAGs).

113 ed of negatively charged glycosaminoglycans (GAGs).

114 iduronic acid containing glycosaminoglycans (GAGs) which are implicated in a number of biological pro

115 ral binding affinity for glycosaminoglycans (GAGs) and reduced viremia levels and the efficiency of r

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

117 us components, including glycosaminoglycans (GAGs).

118 eralization, the role of glycosaminoglycans (GAGs) is less clear.

119 belongs to the group of glycosaminoglycans (GAGs), highly sulfated linear polysaccharides.

120 c fibers, and pooling of glycosaminoglycans (GAGs), with associated losses of medial collagen in the

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

122 GCX breakdown products [glycosaminoglycans (GAGs)] were quantified using dimethylmethylene blue (DMM

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

124 acterization of sulfated glycosaminoglycans (GAGs) by mass spectrometry has long been a formidable an

125 SPG)-associated sulfated glycosaminoglycans (GAGs) that are selectively up-regulated in the tumor mic

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

127 saccharides and sulfated glycosaminoglycans (GAGs).

128 teractions with sulfated glycosaminoglycans (GAGs).

129 eins that carry sulfated glycosaminoglycans (GAGs).

130 Cell surface glycosaminoglycans (GAGs) have been identified as CHIKV attachment factors.

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

132 roteins and cell-surface glycosaminoglycans (GAGs).

133 oupled to binding tissue glycosaminoglycans (GAGs), heparan sulfate (HS), chondroitin sulfate (CS), a

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

135 pled to interaction with glycosaminoglycans (GAGs).

136 larger and produced more glycosominoglycan (GAG) than KGN-only cultures.

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

138 There was profound evidence for a HBD-GAG-HBD stacking configuration.

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

140 rding the structural basis underlying hCXCL1-GAG interactions.

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

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

143 fs of heparan sulfate glycosaminoglycans (HS GAGs) play critical roles in many important biological p

144 sors greatly accelerates the synthesis of HS GAGs, providing key disaccharide and tetrasaccharide int

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

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

147 We analyzed over 670 glycans and identified GAGs as the main glycan bound by CHIKV.

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

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

150 ative deacetylase, Agd3, leads to defects in GAG deacetylation, biofilm formation, and virulence.

151 her there are strain-specific differences in GAG binding are not fully understood.

152 and assessed strain-specific differences in GAG binding capacity.

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

154 CHIKV binding, define strain differences in GAG engagement, and provide further evidence for a criti

155 A. fumigatus glycoside hydrolase involved in GAG synthesis, and PelA, a multifunctional protein from

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

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

158 specimens, the application of CTS increased GAG synthesis, PGE(2) release and MMP activity, with con

159 Increasing GAG sulfation expands the pH range for binding.

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

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

162 :1) effectively suppressed IL-1alpha-induced GAG loss, cell death and inflammatory response significa

163 of hyaluronidase treatment on intramuscular GAG content.

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

165 unctionalizations of synthesized or isolated GAGs are considered.

166 uired for the essential interaction with its GAG receptor(s).

167 ogical data and decreased with applied load; GAG depleted cartilage exhibited higher hydraulic permea

168 and that CHIKV binds most strongly to longer GAG chains of heparin and heparan sulfate.

169 dies provide a powerful approach for mapping GAG-protein interaction networks, revealing new potentia

170 However, mapping GAG-protein interaction networks is challenging as these

171 ntal tissues to determine the role of matrix GAGs in control of mineralization.

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

173 over the culture period and produced minimal GAG.

174 DMMB-GAG and mass spectrometry (MS)-GAG (g/mol creatinine) were increased in CM and UM compa

175 001), with no differences in DMMB-GAG and MS-GAG between CM and UM children or between those with and

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

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

178 ty to obtain informative spectra from native GAG structures.

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

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

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

182 Moreover, administration of GAG protected mice from colitis induced by dextran sulfa

183 Mass spectrometric analysis of GAG isomers, in particular highly sulfated heparin (Hep)

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

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

186 The binding of GAG to ribosomal proteins inhibited cellular translation

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

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

189 Depolymerisation of GAG polysaccharides to oligosaccharides further improved

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

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

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

193 probes for the system-wide identification of GAG-binding proteins in living cells.

194 AG Builder online tool to build 3D models of GAG sequences from GlycoCT codes.

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

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

197 e major capsid protein VP1, a broad range of GAG oligosaccharides bind to recessed regions between VP

198 version of MatrixDB: (i) cross-references of GAG sequences to the GlyTouCan database, (ii) representa

199 e GlyTouCan database, (ii) representation of GAG sequences in different formats (IUPAC and GlycoCT) a

200 arly, lost SMC function and accumulations of GAGs increase mechanical stress on nearby elastic lamell

201 promising for higher throughput analysis of GAGs in complex mixtures.

202 ng and therefore masking the availability of GAGs.

203 er option for structural characterization of GAGs.

204 to provide guidelines for informed choice of GAGs for therapeutic applications.

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

206 further evidence for a critical function of GAGs in CHIKV cell attachment and infection.IMPORTANCE A

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

208 ls new mechanistic insights into the role of GAGs during amyloid fibril formation.

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

210 have focused on a relatively small subset of GAGs - particularly heparin, a readily available, promis

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

212 However, the specific types of GAGs and potentially other glycans to which CHIKV binds

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

214 results also indicate that sulfate groups on GAGs are essential for CHIKV binding and that CHIKV bind

215 stimulation with HIV gp140 protein (ENV) or GAG peptides by multiparameter flow cytometry.

216 ng evidence that for many applications other GAGs are in fact more suitable for regulated and sustain

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

218 differentially mediated by HS but not other GAGs.

219 In SM patients, GAG-DMMB and GAG-MS were increased in those with a fatal

220 cterized by the highest association rate per GAG chain.

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

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

223 mapping of the upper arm muscles to quantify GAG content in patients with post-stroke muscle stiffnes

224 that T(1rho) mapping can be used to quantify GAG content in the muscles of patients with post-stroke

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

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

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

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

229 ransduction (Cx43, AKT), tissue remodelling (GAGs, elastin, collagen) and inflammation (PGE(2), MMPs)

230 n evolution from a Ty3-Gypsy retrotransposon GAG domain.

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

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

233 rlecan heparan sulfate chains than serglycin GAG chains.

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

235 We defined specific GAG components required for CHIKV binding and assessed s

236 ode" and understanding the roles of specific GAG structures in physiology and disease.

237 as these interactions often require specific GAG sulfation patterns and involve transmembrane recepto

238 V, enhance our understanding of the specific GAG moieties required for CHIKV binding, define strain d

239 uid chromatography-tandem mass spectrometry (GAG-MS) assay.

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

241 t to the closely related chondroitin sulfate GAGs.

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

243 nd computational study revealed how sulfated GAG derivatives (sGAG) influence the interplay of vascul

244 The small molecule sulfated GAG antagonist bis-2-methyl-4-amino-quinolyl-6-carbamide

245 ration of surfen as an inhibitor of sulfated GAG signaling to stem GBM invasion.

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

247 The sulfated GAG oligosaccharides derived from cartilage possessed th

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

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

250 Enzymatic removal of cell surface GAGs and genetic ablation that diminishes GAG expression

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

252 mineralization, but to a lesser extent than GAG removal, despite a much larger effect on protein con

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

254 te the same CXCR2 receptor, we conclude that GAG interactions play a role in determining the nature o

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

256 mission electron microscopy (TEM) shows that GAG removal reduced the rate of remineralization in mine

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

258 Collectively, these data demonstrate that GAGs are the preferred glycan bound by CHIKV, enhance ou

259 These results indicate that GAGs promote mineralization in mineralized dental tissue

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

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

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

263 menclature For Glycans) images and (iii) the GAG Builder online tool to build 3D models of GAG sequen

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

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

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

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

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

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

270 lycoproteins and sulfated saccharides on the GAG chain.

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

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

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

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

275 sses of medial collagen in the region of the GAGs.

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

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

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

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

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

281 r both chemokines, the dimer bound all three GAGs with higher affinity than did the monomer, and affi

282 t the binding surfaces for each of the three GAGs were different between the two chemokines.

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

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

285 f five co-expressed genes has been linked to GAG biosynthesis and modification.

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

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

288 The following items related to GAGs have been added in the updated version of MatrixDB:

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

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

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

292 When TGF-beta1 + KGN was used, GAG quantities were similar or slightly greater than the

293 uminate the beneficial properties of various GAGs with reference to specific protein cargoes, and to

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

295 To determine whether GAG binding capacity varies among CHIKV strains, a repre

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

297 While GAG alone promote sprouting, they downregulate VEGF(165)

298 amellar disruption and cellular dropout with GAG production and lost medial collagen that is more pro

299 1 lysine-substituted elastin-like unit) with GAG GM-0111, we created an injectable delivery platform

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

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