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 composed of a core protein covalently linked t

5 HSPGs are necessary to stabilize microtubules in newly f

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

7 HSPGs consist of a core protein with covalently attached

8 HSPGs interact with growth factors and receptors through

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

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

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

12 Perlecan, a HSPG normally confined to the mesangium in mature glomer

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

14 suggesting that the defect involves altered HSPG modification.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 ich can interact with the negatively charged HSPG.

40 sulfate synthesis or sulfation to compromise HSPG function.

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

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

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

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

45 expression of Dlp, but not other Drosophila HSPGs, can restore effectively the tracheal morphogenesi

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

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

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

49 pressure-induced upregulation of endothelial HSPG.

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

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

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

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

54 <0.001); however, the binding affinities for HSPG and c-Met were reduced in GCF and saliva (P <0.002)

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

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

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

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

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

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

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

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

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

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

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

66 Furthermore, HSPGs do not act by transporting extracellular diffusibl

67 Agrin is the predominant GBM-HSPG, but evidence that it contributes to the charge bar

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

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

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

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

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

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

74 ntrolled type 1 diabetes is impaired hepatic HSPG assembly.

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

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

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

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

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

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

81 oxer (extl3) mutants, which are deficient in HSPG synthesis, show laminar targeting defects similar t

82 hamster ovary cells genetically deficient in HSPG.

83 protein uptake is highly dependent on intact HSPG expression.

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

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

86 efficiently bound and infected cells lacking HSPGs if their L2 capsid protein was precleaved by furin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

107 unbranched glycosaminoglycan side chains of HSPGs.

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

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

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

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

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

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

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

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

116 surface localization occurs independently of HSPGs.

117 2 SU and do not express detectable levels of HSPGs, NRP-1, and GLUT-1.

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

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

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

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

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

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

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

125 in epithelial cancer cells were dependent on HSPGs.

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

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

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

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

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

131 age-specific block to GAG synthesis prevents HSPG expression during establishment of the BMP activity

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

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

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

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

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

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

138 -3 (Gpc3) is a heparan sulfate proteoglycan (HSPG) expressed widely during vertebrate development.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 agments or constituents of HS proteoglycans (HSPGs).

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

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

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

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

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

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

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

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

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

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

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

175 LF2 desulfate heparan sulfate proteoglycans (HSPGs) and the HSPG glypican 3 (GPC3) is up-regulated in

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

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

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

179 Heparan sulfate proteoglycans (HSPGs) are extracellular macromolecules found on virtual

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

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

182 Heparan sulfate proteoglycans (HSPGs) are normally associated with the tectal basement

183 Heparan sulfate proteoglycans (HSPGs) are potent regulators of vascular remodeling and

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

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

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

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

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

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 importance of heparan sulfate proteoglycans (HSPGs) in neurodevelopment is becoming increasingly clea

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

202 ed to anionic heparan sulfate proteoglycans (HSPGs) in the glomerular basement membrane (GBM).

203 Heparan sulfate proteoglycans (HSPGs) modulate the action of several of these effector

204 and binds to heparan sulfate proteoglycans (HSPGs) of the basement membrane thereby establishing a h

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 cell-surface heparan sulfate proteoglycans (HSPGs), which have been shown to play major independent

222 uestration by heparin sulfate proteoglycans (HSPGs).

223 cell-surface heparan sulfate proteoglycans (HSPGs).

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

225 clearance via heparan sulfate proteoglycans (HSPGs).

226 ar matrix and heparan sulfate proteoglycans (HSPGs).

227 eracting with heparan sulfate proteoglycans (HSPGs).

228 cell surface heparan sulfate proteoglycans (HSPGs).

229 cell surface heparan sulfate proteoglycans (HSPGs).

230 vivo through heparan sulfate proteoglycans (HSPGs).

231 n mediated by heparan sulfate proteoglycans (HSPGs).

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

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

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

235 However, the relevant HSPG has not been determined.

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

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

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

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

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

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

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

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

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

245 e interaction between virus and cell surface HSPGs.

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

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

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

249 We demonstrate that HSPG glycosaminoglycan levels increased with increasing

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

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

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

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

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

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

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

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

258 cle beginning on page 153) demonstrated that HSPGs under normal physiological conditions are critical

259 embrane and cell surfaces, establishing that HSPGs are the primary attachment factors for these three

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

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

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

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

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

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

266 The HSPG core proteins include the membrane-spanning syndeca

267 eparan sulfate proteoglycans (HSPGs) and the HSPG glypican 3 (GPC3) is up-regulated in HCC, we invest

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

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

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

271 5A signaling, since enzymatic removal of the HSPG backbone resulted in a decrease in cellular Wnt5A l

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

273 lish that transgenic mice overexpressing the HSPG agrin have severe ocular dysgenesis.

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

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

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

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

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

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

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

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

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

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

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

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

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

287 dritic growth of C4da neurons in parallel to HSPGs.

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

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

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

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

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

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

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

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

296 20 promotes the migration of neuroblasts via HSPGs but not S1PR2.

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

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

299 However, the mechanism(s) by which HSPGs control Btl and Htl signaling is unknown.

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