ライフサイエンスコーパス: HSPG

1 HSPG activity is dictated by sulfation patterns controll

2 HSPGs also enhanced FGF2-dependent differentiation, and

3 HSPGs and LAR family receptors are required for sensory

4 HSPGs are necessary to stabilize microtubules in newly f

5 HSPGs are required for Nogo-A-Delta20-induced inhibition

6 HSPGs consist of a core protein with covalently attached

7 nce exists for dysfunction of the syndecan-1 HSPG in diabetic states.

8 The relative expression of DC-SIGN, GLUT-1, HSPGs, and NRP-1 first was examined on both DCs and B-ce

9 rized the interaction of p17 with heparin, a HSPG structural analog, and CXCR1.

10 Therefore, drugs interfering with Abeta-HSPG interactions might be a potential strategy for Alzh

11 Our findings show that acidic pH causes an HSPG-mediated uptake and an enhancement of T cell stimul

12 odified core protein of Dally-like (Dlp), an HSPG required for cell-autonomous Hh response in Drosoph

13 epatocytes; 1K1 and NK1 required heparin, an HSPG analogue, for full agonistic activity.

14 Glypican-3 (GPC3) is an HSPG that is highly expressed in HCC, where it can attra

15 Together, our data reveal an HSPG-dependent pathway that specifically allows dendrite

16 Competition and HSPG digestion experiments suggested mFX- and hFX-enhanc

17 Analysis of free HS and HSPG sugar chains in human serum at the disaccharide lev

18 tylation and N-sulfation in both free HS and HSPG sugar chains were significantly different between p

19 -depth compositional analysis of free HS and HSPG sugar chains.

20 ron extension, mediating CSPG inhibition and HSPG growth promotion.

21 Our findings demonstrate that LRP1 and HSPG function in a cooperative manner to mediate cellula

22 ificantly higher levels of SMAD6, SMAD7, and HSPG mRNAs than controls.

23 m as critical for the contact between SU and HSPG.

24 study was to test the hypothesis that HS and HSPGs are active participators of Abeta pathogenesis in

25 RPTPsigma and HSPGs colocalize in puncta on sensory neurons in culture

26 Heparin, which antagonizes HSPG, significantly inhibited cellular Abeta uptake.

27 Amyloid-associated HSPG can be differentiated from HSPG found in surroundin

28 er, these data show that membrane-associated HSPG can serve as a (co)receptor for some CAV9 and other

29 e with exosomes; however, exosome-associated HSPGs appear to have no direct role in exosome internali

30 not demonstrate a direct correlation between HSPG binding and the potent antiviral activity.

31 ion of Ags with the inherent ability to bind HSPGs pH-dependently.

32 can bind efficiently in the absence of both HSPGs and NRP-1.

33 The SMOC-EC domain bound HSPGs with a similar affinity to BMP2 and could expand t

34 ontext of tumor cell stress was evidenced by HSPG-dependent lipoprotein cell signaling activation thr

35 ich can interact with the negatively charged HSPG.

36 sulfate synthesis or sulfation to compromise HSPG function.

37 tions in RSPO3 residues predicted to contact HSPGs impair its signaling capacity.

38 SULF2 degrades HSPGs by removing 6-O sulfate groups, but had no previou

39 ne whose dysregulation by T2DM would disrupt HSPG structure: the heparan sulfate glucosamine-6-O-endo

40 own of SULF2 in cultured hepatocytes doubled HSPG-mediated catabolism of model remnant lipoproteins.

41 phatase (RPTP) and the only known Drosophila HSPG receptor, for promoting dendritic growth of space-f

42 Although many of the genes that encode HSPG core proteins and the biosynthetic enzymes that gen

43 with combined deletion of the genes encoding HSPG receptors and LDLRs or LRP1.

44 We further demonstrate that endogenous HSPG's are required for the PDGF-AA-guided mesendoderm m

45 pressure-induced upregulation of endothelial HSPG.

46 In incompletely polarized epithelium, HSPG abundance was increased at the AP surface, explaini

47 ypican 3 (GPC3) is the most highly expressed HSPG in hepatocellular carcinoma (HCC).

48 icance of swirling flow on LOX-1 expression, HSPG damage, autophagy and apoptosis in the arterial sys

49 support the view that specific growth factor-HSPG interactions establish morphogen gradients and func

50 <0.001); however, the binding affinities for HSPG and c-Met were reduced in GCF and saliva (P <0.002)

51 immunosorbent assay and binding affinity for HSPG and c-Met using surface plasmon resonance.

52 GF/SF fragment NK1, has reduced affinity for HSPG and exerts proliferative and antiapoptotic effects

53 called 1K1), which have reduced affinity for HSPG.

54 ling in an in vitro assay by competition for HSPG-binding.

55 minate structural determinants important for HSPG and CXCR4 binding by FIV SU and thus further define

56 previously unknown endocytosis mechanism for HSPG-binding cargos in general, which requires forces ge

57 m a second nonconserved domain necessary for HSPG binding, consistent with the observed specificity d

58 o the previously established requirement for HSPG GAG chains in Hh movement, these findings demonstra

59 ng suggested Ad.hFX has greater affinity for HSPGs than does Ad.mFX.

60 tabolism, specifically those responsible for HSPGs sulfurylation, facilitate JEV entry into porcine c

61 erm movement, suggesting an in vivo role for HSPGs in mediating the interaction between PDGF-AA and f

62 d-associated HSPG can be differentiated from HSPG found in surrounding healthy cells and tissues by t

63 ge on the BM allows transfer of virions from HSPG attachment factors to an L1-specific receptor on ba

64 Furthermore, HSPGs do not act by transporting extracellular diffusibl

65 rexpressing the endogenous glycosaminoglycan/HSPG-binding morphogen Decapentaplegic-a transforming gr

66 c, or the other endogenous glycosaminoglycan/HSPG-binding morphogens, Hedgehog and Wingless.

67 fects of host and pathogen glycosaminoglycan/HSPG-binding structures in host survival of infection an

68 As glycosaminoglycans/HSPGs also interact with a number of endogenous secreted

69 entaplegic for binding to glycosaminoglycans/HSPGs during infection and that these bacterial and endo

70 and partially reconstituting (with heparin) HSPG function, we show that mESCs also mechanically sens

71 ntrolled type 1 diabetes is impaired hepatic HSPG assembly.

72 e conclude that clearance of TRLs by hepatic HSPGs is atheroprotective and mediated by multivalent bi

73 tri- to disulfated disaccharides in hepatic HSPGs (P < 0.05).

74 In contrast, the primary defect in hepatic HSPGs in type 2 diabetes appears to arise from accelerat

75 ce that syndecan-1 is the primary hepatocyte HSPG receptor mediating the clearance of both hepatic an

76 ires HSPGs for entry into mouse hepatocytes, HSPGs are dispensable for Ad5 hepatocyte transduction in

77 Here, we identify HSPGs containing a glypican 5 core protein and 2-O-sulfo

78 hamster ovary cells genetically deficient in HSPG.

79 protein uptake is highly dependent on intact HSPG expression.

80 la larvae, we found that dendrites grow into HSPG-deficient areas but fail to stay there.

81 , heparinase, and genetic knockdown of a key HSPG synthetic enzyme, Ext1.

82 t likely initiates interactions with lipids, HSPG, and beta amyloid peptides.

83 To elucidate the relevance of microglial HSPGs in a pro-inflammatory response we isolated microgl

84 We conclude that microglial HSPGs facilitate CD14-dependent TLR4 activation and that

85 TLR4 activation, suggesting that microglial HSPGs facilitate this process.

86 les with long and flexible linkers mimicking HSPG, allowing for effective viral association with a bi

87 iosynthetic enzymes that generate and modify HSPG sugar chains have not yet been analyzed by genetics

88 e-derived cells expressed substantially more HSPGs than the cancer cell lines.

89 se, SULF2, an enzyme that regulates multiple HSPG-dependent RTK signaling pathways, was expressed in

90 ran sulfate (HS) chains attached to multiple HSPGs without diminishing WNT-potentiating activity in c

91 e, the neoPGs assumed the function of native HSPGs, rescued FGF2-mediated kinase activity, and promot

92 e and human retinas and that the addition of HSPG binding to other AAV capsids can increase the numbe

93 is achieved by the translational control of HSPG synthetic enzymes through internal ribosome entry s

94 f tumor selectivity as well as disruption of HSPG function, opening new targets for platinum antitumo

95 We conclude that the primary function of HSPG binding is to enable cell surface furin cleavage of

96 e genetic evidence of a receptor function of HSPG in exosome uptake, which was dependent on intact HS

97 l post-synthetic mechanism for regulation of HSPG function by removing 6S from intact HS chains.

98 The functional relevance of HSPG in the context of tumor cell stress was evidenced b

99 The critical roles of HSPG in cellular Abeta binding and uptake were confirmed

100 The significance of HSPG-pathogen interactions in vivo, however, remains to

101 heterogeneity that underpins the ability of HSPGs to bind with high affinity to many different prote

102 However, the attributes of HSPGs that function as co-receptors for Shh have not yet

103 unbranched glycosaminoglycan side chains of HSPGs.

104 -glycan chains and/or in the distribution of HSPGs may explain the enhanced susceptibility of damaged

105 of SMAD6 and SMAD7 induces the expression of HSPGs, such as SDC1, as well as LDLR, very LDLR, and the

106 have evolved to recognize different forms of HSPGs to enable them to preferentially infect keratinocy

107 ering strategy that exploits the function of HSPGs to promote differentiation in embryonic stem cells

108 Most of the functions of HSPGs are mediated by the variable sulfated glycosaminog

109 he physiological and patterning functions of HSPGs at the Drosophila neuromuscular junction by using

110 olysaccharide chains (glycosaminoglycans) of HSPGs promotes host death and is associated with higher

111 n sulfate (HS) chains, but the importance of HSPGs in liver injury in vivo remains unknown.

112 ves HCMV infection to occur independently of HSPGs and the generation of increased sensitivity to hum

113 surface localization occurs independently of HSPGs.

114 2 SU and do not express detectable levels of HSPGs, NRP-1, and GLUT-1.

115 Here, we show that, in Drosophila, loss of HSPGs differentially affects embryonic Hh, Wg and BMP si

116 between negatively charged sugar moieties of HSPGs and clustered K-T-K motifs in alpha-Syn PFFs.

117 ontrast, at the BL surface, the HS moiety of HSPGs mediated P. aeruginosa binding, cytotoxicity, and

118 h significantly extends the emerging role of HSPGs as key receptors of macromolecular cargo.

119 mprehensive overview of the various roles of HSPGs in these systems and explore the concept of an ins

120 esidues in the highly sulfated subdomains of HSPGs.

121 l of the LD-loaded phenotype by targeting of HSPGs.

122 ay differ from HPV16 in their utilization of HSPGs as their primary attachment factor in vitro.

123 , an enzyme with 6-O-desulfatase activity on HSPGs, is up-regulated in 60% of primary HCCs and is ass

124 in epithelial cancer cells were dependent on HSPGs.

125 l, we found no apparent effect of hypoxia on HSPGs, whereas lipoprotein receptors (VLDLR and SR-B1) w

126 in the same microenvironment do not rely on HSPGs for their dendritic growth.

127 ides showed that peptides targeting CXCR4 or HSPG binding sites can block infection, supporting the V

128 results support a model in which peripheral HSPGs are attractive ligands for LAR receptors on RB neu

129 hat heparan sulfate (HS) proteoglycans (PGs; HSPGs) function as internalizing receptors of cancer cel

130 s, suggesting that syndecan-1 is the primary HSPG mediating hepatic triglyceride clearance.

131 ransduction of CHO mutants unable to produce HSPGs was also curtailed.

132 ox-LDL, inhibits LOX-1 expression, protects HSPG from damage, and decreases both autophagy and apopt

133 action of syndecan-4 (SDC4) HS proteoglycan (HSPG) and KIR2DL4 directly affects receptor endocytosis

134 the syndecan-1 heparan sulfate proteoglycan (HSPG) and the LDL receptor, plus one docking receptor, S

135 ding of AAV to heparan sulfate proteoglycan (HSPG) at the ILM may allow the virus to traverse this ba

136 y regulator of heparan sulfate proteoglycan (HSPG) biosynthesis, is essential for recruiting alpha-Sy

137 -3 (Gpc3) is a heparan sulfate proteoglycan (HSPG) expressed widely during vertebrate development.

138 Heparan sulfate proteoglycan (HSPG) has also been implicated in several pathogenic fea

139 Heparan sulfate proteoglycan (HSPG) is required for this gradient.

140 erved secreted heparan sulfate proteoglycan (HSPG) perlecan, a component of the extracellular matrix.

141 s defective in heparan sulfate proteoglycan (HSPG) production and avoided regions in which HSPGs were

142 bury potential heparan sulfate proteoglycan (HSPG) receptor binding residues within the dimer interfa

143 (LPL), hepatic heparan sulfate proteoglycan (HSPG) receptors, LDLR, or LRP1 and in animals with combi

144 The heparan sulfate proteoglycan (HSPG) syndecan-1 (SDC1) acts as a major receptor for tri

145 CXCL12gamma to heparan sulfate proteoglycan (HSPG) was 10-fold higher than that observed with CXCL12a

146 e GPI-anchored heparan sulfate proteoglycan (HSPG) Wnt co-receptor Dally-like protein (Dlp), cognate

147 ch as DC-SIGN, heparan sulfate proteoglycan (HSPG), and alpha4beta7 integrin, which mediate capture o

148 glypican-type heparan sulfate proteoglycan (HSPG), containing a protein core and attached glycosamin

149 g, we prepared heparan sulfate proteoglycan (HSPG)-knockout (KO) cells by using a clustered regularly

150 extracellular heparan sulfate proteoglycan (HSPG)-specific 6-O-endosulfatases, which regulate a mult

151 gene c-Met and heparan sulfate proteoglycan (HSPG).

152 aran sulfate/heparin class of proteoglycans (HSPG).

153 gh binding to heparan sulfate proteoglycans (HSPG) allowing for possibilities of tumor selectivity as

154 cell surface heparan sulfate proteoglycans (HSPG) and activates LOX-1 dependent autophagy and apopto

155 novel role of heparan sulfate proteoglycans (HSPG) in the adaptive response of tumor cells to hypoxia

156 to lipid and heparan sulfate proteoglycans (HSPG) induces apoE to adopt active conformations for bin

157 Heparan sulfate proteoglycans (HSPG) play a critical role in the interaction of tumor c

158 Cleavage of heparan sulfate proteoglycans (HSPG) with heparinase III prevented infection and BM bin

159 extracellular heparan sulfate proteoglycans (HSPG), suggesting these molecules may be effective targe

160 by mimicking heparan sulfate proteoglycans (HSPG), the highly conserved target of viral attachment l

161 nteracts with heparan sulfate proteoglycans (HSPG).

162 Heparan sulfate (HS) and HS proteoglycans (HSPGs) colocalize with amyloid-beta (Abeta) deposits in

163 agments or constituents of HS proteoglycans (HSPGs).

164 , through the formation of HS proteoglycans (HSPGs).

165 ort that heparan sulfate (HS) proteoglycans (HSPGs) are essential regulators of the germline stem cel

166 surface heparan sulfate (HS) proteoglycans (HSPGs) before pre-S1 engages a specific receptor for upt

167 Heparan sulfate (HS) proteoglycans (HSPGs) bind to multiple growth factors/morphogens and re

168 paran and chondroitin sulfate proteoglycans (HSPGs and CSPGs, respectively) regulate numerous cell su

169 now show that heparan sulfate proteoglycans (HSPGs) act as alternative co-receptors for RSPO3 using a

170 Heparan sulfate proteoglycans (HSPGs) act as binding receptors or attachment factors fo

171 Heparan sulfate proteoglycans (HSPGs) act as coreceptors or storage sites for growth fa

172 ls, p17 binds heparan sulfate proteoglycans (HSPGs) and CXCR1 on leukocytes causing their dysfunction

173 cell surface heparan sulfate proteoglycans (HSPGs) and facilitates entry of bacteria into human epit

174 studies with heparan sulfate proteoglycans (HSPGs) and neuropilin-1 (NRP-1), two molecules important

175 e groups from heparan sulfate proteoglycans (HSPGs) and suppresses uptake of TRLs by cultured hepatoc

176 at HMPV binds heparan sulfate proteoglycans (HSPGs) and that HMPV binding requires only the viral fus

177 ound glypican heparan sulfate proteoglycans (HSPGs) and the secreted protein Shifted (Shf), a member

178 Heparan sulfate proteoglycans (HSPGs) are cell surface receptors that are involved in t

179 Heparan sulfate proteoglycans (HSPGs) are central modulators of developmental processes

180 Heparan sulfate proteoglycans (HSPGs) are concentrated at neuromuscular synapses in man

181 Heparan sulfate proteoglycans (HSPGs) are found in the basement membrane and at the cel

182 Heparan sulfate proteoglycans (HSPGs) are important modulators for optimizing signal tr

183 Heparan sulfate proteoglycans (HSPGs) are synthesised and modified in the Golgi before

184 Heparan sulfate proteoglycans (HSPGs) are ubiquitous components of pathologic amyloid d

185 Heparan sulfate proteoglycans (HSPGs) are ubiquitously expressed molecules that partici

186 ed syndecan-1 heparan sulfate proteoglycans (HSPGs) as remnant lipoprotein receptors.

187 Heparan sulfate proteoglycans (HSPGs) bind to and regulate various tissue injury factor

188 ndependent of heparan sulfate proteoglycans (HSPGs) but, concomitantly, became more sensitive to neut

189 erases modify heparan sulfate proteoglycans (HSPGs) by catalyzing the transfer of a sulfate to a spec

190 Heparan sulfate proteoglycans (HSPGs) control many cellular processes and have been imp

191 Heparan sulfate proteoglycans (HSPGs) critically modulate adhesion-, growth-, and migra

192 ulated by the heparan sulfate proteoglycans (HSPGs) Dally and Dally-like.

193 we show that heparan sulfate proteoglycans (HSPGs) Dally and Syndecan on the surface of epidermal ce

194 Heparan sulfate proteoglycans (HSPGs) function as coreceptors or modulators of Wnt acti

195 In addition, heparan sulfate proteoglycans (HSPGs) have also been implicated in the initiation of Sh

196 Heparan sulfate proteoglycans (HSPGs) have been attributed various roles in inflammatio

197 Heparan sulfate proteoglycans (HSPGs) have long been implicated in a wide range of cell

198 Heparan sulfate proteoglycans (HSPGs) have long unbranched chains of repetitive disacch

199 importance of heparan sulfate proteoglycans (HSPGs) in human papillomavirus (HPV) infection of the mu

200 oproteins and heparan sulfate proteoglycans (HSPGs) in P. aeruginosa-mediated attachment and subseque

201 sociated with heparan sulfate proteoglycans (HSPGs) metabolism, specifically those responsible for HS

202 PV16 binds to heparin sulfate proteoglycans (HSPGs) on either the epithelial cell surface or basement

203 gregates bind heparan sulfate proteoglycans (HSPGs) on the cell surface to transmit pathologic proces

204 teins to form heparan sulfate proteoglycans (HSPGs) on the cell surface.

205 Heparan sulfate proteoglycans (HSPGs) play critical roles in the distribution and signa

206 Heparan sulfate proteoglycans (HSPGs) regulate a number of major developmental processe

207 also contains heparan sulfate proteoglycans (HSPGs) that may contribute to amyloid formation by bindi

208 cell surface heparan sulfate proteoglycans (HSPGs) to infect host cells in vitro.

209 rter, GLUT-1, heparan sulfate proteoglycans (HSPGs), and neuropilin-1 (NRP-1) were demonstrated to fa

210 s that modify heparan sulfate proteoglycans (HSPGs), are essential to regulate neuronal migration and

211 expression of heparan sulfate proteoglycans (HSPGs), including TbetaRIII, GPC1, GPC3, SDC3, and SDC4,

212 ous family of heparan sulfate proteoglycans (HSPGs), is expressed by cells of the hematopoietic syste

213 Heparan sulfate proteoglycans (HSPGs), located on the cell surface or in the extracellu

214 RNAs encoding heparan sulfate proteoglycans (HSPGs), particularly SDC1 mRNA, and cell surface levels

215 ndependent of heparan sulfate proteoglycans (HSPGs), suggesting that evasion of DIDS lowered dependen

216 ional role of heparan sulfate proteoglycans (HSPGs), the importance of chondroitin sulfate proteoglyc

217 specifically, heparan sulfate proteoglycans (HSPGs), were resistant to binding and infection by HMPV.

218 ESCs involves heparan sulfate proteoglycans (HSPGs), which have also been shown to transduce shear st

219 n mediated by heparan sulfate proteoglycans (HSPGs).

220 uestration by heparin sulfate proteoglycans (HSPGs).

221 cell-surface heparan sulfate proteoglycans (HSPGs).

222 Wg) depend on heparan sulfate proteoglycans (HSPGs).

223 clearance via heparan sulfate proteoglycans (HSPGs).

224 ar matrix and heparan sulfate proteoglycans (HSPGs).

225 eracting with heparan sulfate proteoglycans (HSPGs).

226 cell surface heparan sulfate proteoglycans (HSPGs).

227 cell surface heparan sulfate proteoglycans (HSPGs).

228 vivo through heparan sulfate proteoglycans (HSPGs).

229 ing of Vn to heparan-sulfated proteoglycans (HSPGs).

230 blished that heparan sulphate proteoglycans (HSPGs) are required for signalling by key developmental

231 ors, but the molecular mechanisms regulating HSPG function are poorly understood.

232 However, the relevant HSPG has not been determined.

233 e onset of Hh and Wg signaling which require HSPGs.

234 We conclude that while AAV2 requires HSPGs for entry into mouse hepatocytes, HSPGs are dispen

235 Crystallographic analyses of a shared HSPG-CSPG binding site reveal a conformational plasticit

236 ent of neuroblastoma cell lines with soluble HSPGs promoted neuroblast differentiation via FGFR1 and

237 Although the roles of specific HSPG modifications have been described in cell culture a

238 Previous studies indicate that SU-HSPG interactions occur within the V3 loop.

239 the role of syndecan-1, a major cell surface HSPG of epithelial cells, in Staphylococcus aureus corne

240 e role of syndecan-1, the major cell-surface HSPG of hepatocytes, in AILI.

241 Further, enzymatic depletion of cell-surface HSPG or pharmacological inhibition of endogenous PG bios

242 e interaction between virus and cell surface HSPGs.

243 erating structural diversity of cell surface HSPGs; this activity provides an important mechanism to

244 lized exosomes colocalized with cell-surface HSPGs of the syndecan and glypican type, and exosome upt

245 Here, we demonstrate that HSPG and LRP1 cooperatively mediate cellular Abeta uptak

246 We demonstrate that HSPG glycosaminoglycan levels increased with increasing

247 We show that HSPG binding is correlated with greater accumulation and

248 We further showed that HSPG is more important for the binding of Abeta to the c

249 Our data support the emerging view that HSPG functions are not limited to the cell surface and m

250 We conclude that HSPGs are RSPO co-receptors that potentiate WNT signalin

251 We conclude that HSPGs may have an important role in the adaptive respons

252 These data demonstrate that HSPGs are important cellular attachment factors for AKAV

253 The data also demonstrate that HSPGs are required for hepatocyte transduction by AAV2.

254 We further demonstrate that HSPGs potentiate Wnt5A signaling, since enzymatic remova

255 was genetically abolished, demonstrated that HSPGs are not likely to function as hepatocyte Ad5 recep

256 We provide biochemical evidence that HSPGs are sorted to and associate with exosomes; however

257 We propose that HSPGs define the physical space of the niche by serving

258 We previously showed that HSPGs expressed on the surface of APCs can serve as rece

259 vertebrates, recent studies have shown that HSPGs do indeed mediate a wide range of functions in ear

260 The findings suggest that HSPGs contribute to amyloid deposition in tgSwe mice by

261 ic physiology and morphology suggesting that HSPGs function both presynaptically and postsynaptically

262 The HSPG core proteins include the membrane-spanning syndeca

263 Conversely, the HSPG-binding domains of RSPO3 can be entirely replaced w

264 We thereby identify the HSPG family members syndecan-3 and syndecan-4 as functio

265 We introduced a T132R substitution into the HSPG-nonbinding strain Griggs and recovered infectious v

266 ies of nested V3 peptides to further map the HSPG binding sites and found that both sides of the pred

267 5A signaling, since enzymatic removal of the HSPG backbone resulted in a decrease in cellular Wnt5A l

268 present study, we have profiled each of the HSPG core proteins in HCV attachment.

269 These HSPG co-receptors are expressed by cerebellar granule ce

270 At the subcellular level, these HSPG co-receptors are located adjacent to the primary ci

271 receptors may also become activated through HSPG/growth factor/HPV16 complexes that initiate signali

272 dapted [TCA]) such as FIV-34TF10 can bind to HSPG, whereas SU from field strains (FS) such as FIV-PPR

273 B2, B3, and B23) showed decreased binding to HSPG but increased anti-HIV activity.

274 ignated gammaB1) showed increased binding to HSPG but reduced anti-HIV activity.

275 ed that pH decrease allows CRM197 binding to HSPG-expressing cells, including APCs.

276 Thus, Shh binds to HSPG co-receptors containing a glypican 5 core and 2-O-s

277 differences in Ad.hFX and Ad.mFX affinity to HSPGs may result in differences in their ability to enha

278 Interference with tau binding to HSPGs prevents recombinant tau fibrils from inducing int

279 Along with binding to HSPGs, HPV16 binds to alpha6 integrins, which initiate f

280 After binding to HSPGs, the virion undergoes conformational changes, lead

281 upport a model in which attachment of HBV to HSPGs is mediated by the AGL HS binding site, including

282 dritic growth of C4da neurons in parallel to HSPGs.

283 antagonize the binding of these pathogens to HSPGs and stop their cellular internalization, but the a

284 zing binding of heparin-binding pathogens to HSPGs.

285 decreased binding of ApoE-deficient TRLs to HSPGs on human hepatoma cells, and decreased clearance o

286 apsid hexon protein and bridges the virus to HSPGs on the cell surface.

287 knockdowns, we found that the transmembrane HSPG Syndecan 2 (Sdc2) regulates LR patterning through c

288 ts identify an Mmp mechanism that fine-tunes HSPG co-receptor function to modulate Wnt signaling to c

289 nclude that cancer cell-derived exosomes use HSPGs for their internalization and functional activity,

290 find that tau fibril uptake also occurs via HSPG binding.

291 gly, we show that Nogo-A-Delta20 can act via HSPGs independently of its receptor, Sphingosine-1-Phosp

292 lycation-bearing cargos that enter cells via HSPGs.

293 neurons and Nogo-A-responsive cell lines via HSPGs.

294 20 promotes the migration of neuroblasts via HSPGs but not S1PR2.

295 SCs also mechanically sense shear stress via HSPGs to modulate Fgf5 expression.

296 f positive charges as one mechanism by which HSPG binding can be achieved.

297 SPG) production and avoided regions in which HSPGs were locally degraded.

298 fied by tissue morphology, interactions with HSPG, and Lrp5-mediated receptor binding, to regulate ze

299 ggests that retention of an interaction with HSPGs during the entry process in vivo may be evolutiona

300 ed dependence on an initial interaction with HSPGs.