ライフサイエンスコーパス: hyaluronan

1 required that did not include degrading the hyaluronan.

2 erequisite for local, cell-based turnover of hyaluronan.

3 alized more readily than high molecular mass hyaluronan.

4 mor without depletion of stromal collagen or hyaluronan.

5 n asymmetrical bubble collapse may break the hyaluronan.

6 es may be related to associated increases in hyaluronan.

7 on of the extracellular matrix macromolecule hyaluronan.

8 CBMs and complementary to its acidic ligand, hyaluronan.

9 maller stimulatory effects than reacetylated hyaluronan.

10 se expression and decreased the retention of hyaluronan.

11 s maintained by high autocrine production of hyaluronan.

12 ently conjugate different peptide species to hyaluronan.

13 post-coitum, where it was co-localized with hyaluronan.

14 compared our results to chemically sulfated hyaluronan.

15 ated by the recognition of leukocyte-derived hyaluronan.

16 it is used for defining functions related to hyaluronan.

17 oordinate loss in another glycosaminoglycan, hyaluronan.

18 MSO), 15% human serum albumin (HSA) and 0.1% hyaluronans.

19 Hyaluronan, a high molecular mass glycosaminoglycan, has

20 Hyaluronan, a major epidermal extracellular matrix compo

21 mino-acid peptide of human origin that binds hyaluronan, a major macromolecular component of the eye'

22 Hyaluronan, a major matrix molecule in epidermis, is oft

23 Finally, we found that the digestion of hyaluronan, a principal extracellular matrix component,

24 ryos exhibit increased cell density, reduced hyaluronan accumulation and impaired protein glycosylati

25 Furthermore, FGFR-mediated hyaluronan accumulation requires activation of the STAT3

26 ndicating reduced confinement by neighboring hyaluronan-aggrecan complexes.

27 role but must act together with the others: hyaluronan, anchored at the outer surface of articular c

28 (ii) that heparin inhibits the intracellular hyaluronan and autophagy responses, but after completing

29 tor (TNF)-stimulated gene-6 (TSG-6) binds to hyaluronan and can reorganize/stabilize its structure, a

30 ndroitin sulfate of inter-alpha-inhibitor to hyaluronan and consequently to matrix stabilization.

31 thases; the resulting 4-N3-GlcNAc-terminated hyaluronan and heparosan were then successfully conjugat

32 er a previously unsuspected mechanism of how hyaluronan and Hyal-2 control platelet generation.

33 nd TGFbeta, downstream protumor factors, and hyaluronan and its cofactor TSG6, which all contribute t

34 an receptor CD44 mediates the endocytosis of hyaluronan and its delivery to endosomes/lysosomes.

35 regulate secretion of essential lubricants (hyaluronan and lubricin) and cytokines from synovial fib

36 ooth muscle alpha-actin, laminin alpha1, and hyaluronan and proteoglycan link protein 1 (Hapl1) produ

37 Here, we report that hyaluronan and proteoglycan link protein 1 (HAPLN1) is p

38 matic targeting of the proteoglycan versican/hyaluronan and proteoglycan link protein 1 rich myxoid m

39 rsican and its linking protein, a vertebrate hyaluronan and proteoglycan link protein 1.

40 and living human keratinocytes, to localize hyaluronan and sialylation sites.

41 e achieved through the addition of exogenous hyaluronan and the proteoglycan versican, but this was n

42 tein that stabilizes the interaction between hyaluronan and versican and is expressed in endocardial

43 Finally, the expansion of a hyaluronan and versican-rich matrix was observed upon re

44 ance of rHpScs consisting of a substratum of hyaluronans and Kubota's medium (KM), a serum-free mediu

45 d the pericellular coat and the retention of hyaluronan, and decreased cell adhesion in a dose-depend

46 D-glucuronic acid (GlcA), a substructure of hyaluronan, and N-acetylneuraminic acid (NANA), the most

47 x enriched in elastic fibers and depleted in hyaluronan, and reduction of the proinflammatory cell su

48 vement of disturbed flow and of neutrophils, hyaluronan, and Toll-like receptor 2 ligation in superfi

49 Low molecular mass hyaluronans are known to induce inflammation.

50 This is especially true in cartilage, where hyaluronan assembles into an aggregate structure with th

51 increases with UDP-sugars, and HAS3 produces hyaluronan at high speed even with minimum substrate con

52 d in extracellular matrix remodeling such as hyaluronan, biglycan, and fibronectin.

53 or the expansion of mouse COCs in vitro, the hyaluronan-binding function of TSG-6 does not play a maj

54 -6 mutants (with impaired transferase and/or hyaluronan-binding functions) revealed that although the

55 Proteolysis of versican generates a hyaluronan-binding G1 domain.

56 HABP2 (hyaluronan-binding protein 2) is a Ca(2+)-dependent seri

57 n, we have found that the well characterized hyaluronan-binding site in the TSG-6 Link module is not

58 ethylumbelliferone, as a potent inhibitor of hyaluronan biosynthesis, due in part to its ability to s

59 thylumbelliferone was indeed an inhibitor of hyaluronan biosynthesis, this depletion did not give ris

60 UTP increased hyaluronan both in the pericellular matrix and in the cu

61 d reduction in IL-6 and a 5-fold decrease in hyaluronan, both linked to lung fibrosis and PH, were al

62 the extracellular proteolytic processing of hyaluronan-bound proteoglycan.

63 P6 also inhibited cell adhesion to hyaluronan but had no effect on adhesion to VCAM-1 (alph

64 g region to chondroitin sulfate and sulfated hyaluronan but not to the non-sulfated hyaluronan, confi

65 TGFbeta signaling, whereas the reduction in hyaluronan cable formation induced by V3 expression is m

66 razinolysis resulted in bond cleavage of the hyaluronan chain causing a reduction of the molecular ma

67 However, the addition of intact aggrecan to hyaluronan chains sonicated for 5 and 10 s reblocked the

68 with IL-1beta changes the structure of their hyaluronan coat by influencing the amount, post-translat

69 e1, antibody blockade or depletion of the DC hyaluronan coat not only delayed lymphatic trafficking o

70 -1beta turns on the monocyte adhesion of the hyaluronan coat on human keratinocytes.

71 Here we show, unexpectedly, that hyaluronan compresses vessels only in collagen-rich tumo

72 fated hyaluronan but not to the non-sulfated hyaluronan, confirming binding specificity.

73 iae, the recognition and degradation of host hyaluronan contributes to bacterial spreading through th

74 ptor for the glycosaminoglycan ECM component hyaluronan, coordinates the motility and proliferative r

75 Instead, we found that the increase in the hyaluronan-dependent monocyte binding was associated wit

76 eased monocyte binding to keratinocytes in a hyaluronan-dependent way.

77 Hyaluronan depletion also increases the fraction of the

78 The other partially N-acylated hyaluronan derivatives tested showed smaller stimulatory

79 the overall size of the aggregate prevented hyaluronan endocytosis and furthermore that proteolysis

80 These data suggest that hyaluronan endocytosis is regulated in large part by the

81 a size range of aggrecan exists that permits hyaluronan endocytosis.

82 In conclusion, hyaluronan exacerbates CNS autoimmunity, enhances enceph

83 d partially butyrylated lower molecular mass hyaluronans exert their effects through the TLR-4 recept

84 The HAS2 product hyaluronan further stimulated CD44s-mediated Akt signali

85 cilitate simple synthesis of multifunctional hyaluronan graft polymers, thus enabling novel approache

86 The extracellular matrix polysaccharide hyaluronan (HA) accumulates at sites of autoimmune infla

87 adenocarcinoma is characterized by excessive hyaluronan (HA) accumulation in the tumor microenvironme

88 Hyaluronan (HA) accumulation into artery walls supports

89 ning variable exon 6 (CD44v6) and its ligand hyaluronan (HA) alter cellular function in response to i

90 to WT mice also revealed that expression of hyaluronan (HA) and activation of hyaluronan synthase-2

91 espect to the extracellular matrix component hyaluronan (HA) and chemokine expression.

92 Elevated expression of hyaluronan (HA) and HA receptors, receptor for HA-mediat

93 e an extracellular matrix (ECM), enriched in hyaluronan (HA) and its binding partner versican, which

94 by accumulation of a pericellular matrix of hyaluronan (HA) and the HA-dependent co-localization of

95 s of the extracellular matrix polysaccharide hyaluronan (HA) are characteristic of autoimmune insulit

96 Selective inhibitors of hyaluronan (HA) binding to the cell surface receptor CD4

97 y stimuli by synthesizing leukocyte-adhesive hyaluronan (HA) cables that remain attached to their cel

98 The hyaluronan (HA) capsule of GAS has been proposed to prot

99 smembrane receptor for the glycosaminoglycan hyaluronan (HA) demonstrate a number of neurological dis

100 sma membrane, where they extrude the growing hyaluronan (HA) directly into cell surface and extracell

101 icance of endogenous innate ligands, such as hyaluronan (HA) fragments, in clinical or experimental l

102 Increased synthesis of cervical hyaluronan (HA) from early to late pregnancy has long be

103 The breakdown and release of hyaluronan (HA) from the extracellular matrix has been h

104 LYVE-1 has been implicated in both uptake of hyaluronan (HA) from tissue matrix and in facilitating t

105 The matrix polysaccharide hyaluronan (HA) has a critical role in the expansion of

106 ssels, accompanied by accumulation of low-MW hyaluronan (HA) in mouse orthotopic allografts undergoin

107 Importantly, matrix hyaluronan (HA) induces the up-regulation of stem cell m

108 Hyaluronan (HA) inhibits OPC maturation and complexes wi

109 Hyaluronan (HA) is a large (>1500 kDa) polysaccharide of

110 Hyaluronan (HA) is a major component of this structure.

111 Hyaluronan (HA) is a major glycosaminoglycan component o

112 Hyaluronan (HA) is a structurally simple polysaccharide,

113 Hyaluronan (HA) is an extracellular matrix glycosaminogl

114 During inflammation, hyaluronan (HA) is increased at sites of inflammation wh

115 Hyaluronan (HA) is present in the extracellular matrix o

116 in the interstitium of high-molecular-weight hyaluronan (HA) is principally responsible for generatin

117 Hyaluronan (HA) is required for endothelial-to-mesenchym

118 Hyaluronan (HA) is synthesized by three HA synthases (HA

119 Hyaluronan (HA) is the major glycosaminoglycan in the ex

120 ersican bound to a heavy chain (HC)-modified hyaluronan (HA) matrix (HC-HA).

121 Hyaluronan (HA) may have proinflammatory roles in the co

122 )-dependent signaling pathway that regulates hyaluronan (HA) metabolism and drives adult fibroblasts

123 We previously reported an altered hyaluronan (HA) metabolism in idiopathic pulmonary arter

124 angiogenic drug quininib was formulated into hyaluronan (HA) microneedles whose safety and efficacy w

125 tumor necrosis factor-stimulated gene 6), to hyaluronan (HA) oligosaccharides is an irreversible even

126 d the extracellular matrix glycosaminoglycan hyaluronan (HA) on AEC2s are important for AEC2 renewal,

127 In response to tissue injury, hyaluronan (HA) polymers are cleaved by host hyaluronida

128 We present data that hyaluronan (HA) polysaccharides, about 14-86 monosacchar

129 Hyaluronan (HA) produced by HAS3 is a ubiquitous compone

130 Hyaluronan (HA) promotes transforming growth factor (TGF

131 The hyaluronan (HA) receptor for endocytosis (HARE; Stab2) c

132 The human hyaluronan (HA) receptor for endocytosis (HARE; the 190-

133 Hyaluronan (HA) turnover accelerates metastatic progress

134 HCs) from inter-alpha-inhibitor (IalphaI) to hyaluronan (HA) via the protein product of tumor necrosi

135 to study the interaction of the GAG polymer hyaluronan (HA) with CD44, its receptor in vascular endo

136 n.SIGNIFICANCE STATEMENT We demonstrate that hyaluronan (HA) with different molecular weights produce

137 Heavy chain (HC)-hyaluronan (HA), a complex formed by the covalent linkag

138 ed DC culture based on their ability to bind hyaluronan (HA), a major component of the extracellular

139 Hyaluronan (HA), a major component of the extracellular

140 We are interested in the role that hyaluronan (HA), an extracellular matrix molecule synthe

141 We have identified a novel role for hyaluronan (HA), an extracellular matrix polymer, in gov

142 lular hyaluronate lyase (HL), which degrades hyaluronan (HA), chondroitin 6-sulfate, and dermatan sul

143 r inter-alpha-inhibitor heavy chains (HC) to hyaluronan (HA), facilitating HA receptor binding.

144 For each class of the glycosaminoglycans-hyaluronan (HA), heparan sulfate/heparin (HS/HP), chondr

145 which exhibited significant activity against hyaluronan (HA), poly-beta-d-glucuronic acid (poly-GlcUA

146 Our model is focused on the damage in hyaluronan (HA), which is the main structural component

147 gene-6 (TSG-6) is an inflammation-associated hyaluronan (HA)-binding protein that contributes to remo

148 oocytes are surrounded by a highly hydrated hyaluronan (HA)-rich extracellular matrix with embedded

149 ntified in extracts from the dermis in which hyaluronan (HA)-versican-fibrillin complexes are found.

150 the high molecular weight glycosaminoglycan, hyaluronan (HA).

151 presence or absence of a CD44-specific Ab or hyaluronan (HA).

152 milar to LPS, whereas partially deacetylated hyaluronan had no stimulatory effect, indicating the cri

153 liated apical surfaces to form a heavy chain hyaluronan (HC-HA) matrix in the absence of inflammatory

154 cans, biglycan), and glycosaminoglycans (eg, hyaluronan, heparan sulfate) are upregulated on cardiac

155 ccharides, including cello-oligosaccharides, hyaluronan, heparan sulfate, heparin, and chondroitin su

156 ucts were then tested for incorporation into hyaluronan, heparosan, or chondroitin using polysacchari

157 hondroitin sulfate and high-molecular-weight hyaluronan (HMW-HA) associated with IAIP.

158 yperalgesia induced by high molecular weight hyaluronan (HMWH).

159 Hyaluronan (hyaluronic acid; HA) instillation to the bla

160 vels or distribution of sialic acids (SA) or hyaluronan in animal cells are indicators of pathologica

161 ce of versican was not only synergistic with hyaluronan in increasing cell proliferation, but the dep

162 e as follows: 1) heparin blocks synthesis of hyaluronan in intracellular compartments, which prevents

163 e of the acetyl groups of low molecular mass hyaluronan in stimulating the production of proinflammat

164 hesis or increase the amount of pericellular hyaluronan in these cells.

165 d all sulfated GAGs, but not the nonsulfated hyaluronan, indicating that binding is specific to the p

166 ugh a mechanism preceding and independent of hyaluronan inhibition.

167 ontrolled by the affinity of individual CD44-hyaluronan interactions.

168 e aggrecan monomer was required to allow for hyaluronan internalization.

169 erentially bind to YKL-40 over collagen, and hyaluronan is likely the preferred physiological ligand,

170 In most extracellular matrices hyaluronan is not present as a free polysaccharide but o

171 Hyaluronan is organized into a cross-linked network by t

172 In vertebrates, hyaluronan is produced in the plasma membrane from cytos

173 urthermore, we identified that HAS2-produced hyaluronan is required for CD44V6 and TGFbetaRI co-local

174 Hyaluronan is the predominant glycosaminoglycan componen

175 tly attributed to deposition of collagen and hyaluronan, leading to interstitial hypertension collaps

176 decreases both FGFR-driven tumor growth and hyaluronan levels within the tumor.

177 Hyaluronidase (Hyal) and low m.w. hyaluronan (LMW HA) fragments have been widely reported

178 have demonstrated that low molecular weight hyaluronan (LMW-HA, approximately 2500 Da) promotes endo

179 Low molecular weight hyaluronan (LMWH) acts at both peptidergic and nonpeptid

180 e mechanism of chondrocyte activation due to hyaluronan loss, a depletion method was required that di

181 Hyaluronan, lubricin and phospholipids, molecules ubiqui

182 rmation of a monocyte-adhesive extracellular hyaluronan matrix after completing cell division.

183 rmation of a monocyte-adhesive extracellular hyaluronan matrix after completing cell division; and (i

184 ipogenic pathway that induces synthesis of a hyaluronan matrix that recruits inflammatory cells and e

185 ays of culture, and form a monocyte-adhesive hyaluronan matrix through an endoplasmic reticulum stres

186 collagen matrices, a large accumulation of a hyaluronan matrix within the trabecular bone marrow, and

187 influxed macrophages effectively remove the hyaluronan matrix without inducing pro-fibrotic response

188 e accumulation of autophagic RMCs, increased hyaluronan matrix, and influx of macrophages over 6 week

189 the formation of a larger monocyte-adhesive hyaluronan matrix.

190 much larger extracellular monocyte-adhesive hyaluronan matrix.

191 adipocytes and macrophages embedded in this hyaluronan matrix.

192 The adjunctive application of hyaluronan may have positive effects on PD reduction and

193 c vessels and transited to the lumen through hyaluronan-mediated interactions with the lymph-specific

194 Here we report that the hyaluronan-mediated motility receptor (HMMR) is highly e

195 the previously reported rapid activation of hyaluronan metabolism in response to tissue trauma or ul

196 tissue repair is dependent on regulation of hyaluronan metabolism via fibroblast-specific STAT3 sign

197 adder urothelial layer and the expression of hyaluronan-metabolizing enzymes and/or HA receptors in K

198 in gel, fibrin-Matrigel mixed gel and fibrin-hyaluronan mixed gel, were investigated to optimize the

199 that the CD44, a transmembrane receptor for hyaluronan, modulates synaptic plasticity.

200 We find that surface-anchored hyaluronan molecules complex synergistically with phosph

201 rified aggrecan was added to FITC-conjugated hyaluronan, no internalization of hyaluronan was detecte

202 , HAS1 transfection reduced the synthesis of hyaluronan obtained by HAS2 and HAS3, suggesting functio

203 It was also determined that sonicated hyaluronan of smaller molecular size was internalized mo

204 diated by the extracellular matrix component hyaluronan of very high molecular weight (HMW-HA).

205 a, TNFalpha, LPS, fibronectin fragments, and hyaluronan oligosaccharides.

206 LTalpha in HRS cells and tissue stroma; and hyaluronan on endothelial cells are readily detected in

207 served as a chain termination substrate for hyaluronan or heparosan synthases; the resulting 4-N3-Gl

208 t on cytokine production by the reacetylated hyaluronan or LPS but had no stimulatory effect of its o

209 s to prototypical damage molecules, HMGB1 or hyaluronan, or to necrotic cells; although they secreted

210 Heavy chain-Hyaluronan/Pentraxin 3 (HC-HA/PTX3) is a complex purifie

211 Modulation of hyaluronan polymer size is responsible for its control o

212 Our results suggest that chitohexaose and hyaluronan preferentially bind to YKL-40 over collagen,

213 was associated with an increase in bacterial hyaluronan production (mucoid colonies 200 mug per CFU a

214 , the number of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1(+)) macrophages decreased

215 ion profiles of lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), a biomarker that plays c

216 ing podoplanin, lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1), and cluster of different

217 podoplanin and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1).

218 ls that express lymphatic vessel endothelial hyaluronan receptor 1 (LYVE1), which include lymphatic e

219 ssion, and more lymphatic vessel endothelial hyaluronan receptor 1-positive vascular endothelial grow

220 We further show that the hyaluronan receptor CD44 interacts with both PDGFRbeta a

221 In many cells hyaluronan receptor CD44 mediates the endocytosis of hya

222 multilayered spheroid cells and express the hyaluronan receptor CD44, as well as stem cell factor re

223 We investigated the functional role of hyaluronan receptor CD44V6 (CD44 containing variable exo

224 Overexpression of the hyaluronan receptor HMMR in primary LUAD was associated

225 Sprague Dawley rats, the role of the cognate hyaluronan receptor, CD44 signaling in the antihyperalge

226 broblasts have high endogenous levels of the hyaluronan receptor, CD44V6 (CD44 variant containing exo

227 traits, including in regions of p53, and the hyaluronan receptors CD44 and HMMR (RHAMM).

228 Hyaluronan release and dispersion of the cumulus cells p

229 s experimentally depleted of cell-associated hyaluronan respond by switching to a pro-catabolic metab

230 se cells are retained around the oocyte by a hyaluronan-rich extracellular matrix synthesized before

231 nating and stabilizing the formation of this hyaluronan-rich matrix.

232 l survival, and micrometastasis expansion in hyaluronan-rich microenvironments in the lung and brain

233 Hence, cells equipped with hyaluronan-rich PCM can in principle manipulate surface

234 chanisms involves the formation of extended, hyaluronan-rich pericellular coats on local fibroblasts,

235 The hyaluronan-rich pericellular matrix (PCM) plays physical

236 The pericellular matrix is a robust, hyaluronan-rich polymer brush-like structure that contro

237 We propose that a hyaluronan-rich, relatively immobile gel-fluid phase ind

238 gical ligand, because the negatively charged hyaluronan shows enhanced affinity for YKL-40 over neutr

239 lectively N-butyrylated lower molecular mass hyaluronan shows promise as an example of a novel semisy

240 Butyrylated hyaluronan significantly reduced the stimulatory effect

241 show that the N-terminal module of Hyl is a hyaluronan-specific carbohydrate-binding module (CBM) an

242 Hyaluronan staining in the glomeruli of heparin-treated

243 rs displayed significantly less versican and hyaluronan staining, had lower volumes, and had reduced

244 The reacetylated hyaluronan stimulated proinflammatory cytokine productio

245 Hyaluronan suppressed production of CXCL12, whereas 4MU

246 Collagen I (COL1A1), collagen III (COL3A1), hyaluronan synthase (HAS) 2, and fibronectin expression

247 wn products UDP and UMP act as mediators for hyaluronan synthase (HAS) activation in human epidermal

248 brane from cytosolic UDP-sugar substrates by hyaluronan synthase 1-3 (HAS1-3) isoenzymes that transfe

249 STAT3 pathway, which regulates expression of hyaluronan synthase 2 (HAS2) and subsequent hyaluronan s

250 We identified hyaluronan synthase 2 (Has2) as another novel downstream

251 In addition, we found that expression of hyaluronan synthase 2 (Has2) was elevated by a loss of S

252 tures induced a specific, rapid induction of hyaluronan synthase 2 (HAS2), and an increase of hyaluro

253 ntricular canal marker genes, such as tbx2b, hyaluronan synthase 2 (has2), notch1b and bmp4, are chan

254 ynovial cells, and condyles displayed higher Hyaluronan synthase 2 expression.

255 Furthermore, TBX4 regulated hyaluronan synthase 2 production to enable fibroblast in

256 Both Irinotecan/HAS2 (Hyaluronan synthase 2) and Bevacizumab/PGAM1 (Phosphogly

257 e identified a common SNP, rs2232228, in the hyaluronan synthase 3 (HAS3) gene that exerts a modifyin

258 ion, but the depletion of versican decreased hyaluronan synthase expression and decreased the retenti

259 ice isoform CD44s promoted expression of the hyaluronan synthase HAS2 by activating the Akt signaling

260 llular UDP-glucuronic acid and inhibition of hyaluronan synthase transcription.

261 ression of hyaluronan (HA) and activation of hyaluronan synthase-2 (Has2) are also enhanced upon PN/I

262 oblasts revealed induction of IL8, SERPINB2, hyaluronan synthase-2, and other genes associated with t

263 egulated HAS2 expression, although the other hyaluronan synthases (HAS1, HAS3) and hyaluronidases (HY

264 Hyaluronan synthases (HAS1-3) are unique in that they ar

265 hows that heparin inhibits the intracellular hyaluronan synthesis and autophagy responses, but at the

266 Increased hyaluronan synthesis and CD44 expression have been detec

267 over cellular functions, and the balance of hyaluronan synthesis and degradation determines its mole

268 ecifically, we found that NOX4/ROS regulates hyaluronan synthesis and the transcription of CD44V6 via

269 signals for epidermal inflammation, enhanced hyaluronan synthesis as an integral part of it.

270 nses, but after completing division, induces hyaluronan synthesis at the plasma membrane with the for

271 n the extracellular matrix and that blocking hyaluronan synthesis decreases proliferation, migration,

272 dy was to investigate the role of endogenous hyaluronan synthesis during myogenesis.

273 4MU decreased hyaluronan synthesis in vitro and in vivo.

274 therapies inhibiting both FGFR activity and hyaluronan synthesis is more effective than targeting ei

275 IL-1beta did not influence hyaluronan synthesis or increase the amount of pericellu

276 hyperglycemic medium initiate intracellular hyaluronan synthesis that induces autophagy and the cycl

277 hyperglycemic medium initiate intracellular hyaluronan synthesis that induces autophagy/cyclin D3-in

278 As similar insults are known to activate hyaluronan synthesis we explored the possibility that ex

279 Inhibition of hyaluronan synthesis with 4MU protects against an animal

280 at oncogenic Ras regulates CD147 expression, hyaluronan synthesis, and formation of CD147-CD44-EGFR c

281 In hyaluronan synthesis-blocked cultures, restoration of th

282 ntially important functional consequences on hyaluronan synthesis.

283 hyaluronan synthase 2 (HAS2) and subsequent hyaluronan synthesis.

284 uronan synthase 2 (HAS2), and an increase of hyaluronan synthesis.

285 - 1.5% respectively, whereas for butyrylated hyaluronan, the total NH2, N-acetyl, and N-butyryl moiet

286 g of the extracellular matrix polysaccharide hyaluronan to its main cell surface receptor CD44 is con

287 transfer of IalphaI heavy chains (HCs) onto hyaluronan (to form covalent HC.HA complexes that are cr

288 n-rich tumours, suggesting that collagen and hyaluronan together are critical targets for decompressi

289 ation in the stroma of the glycosaminoglycan hyaluronan, together with the large gel-fluid phase and

290 ssion of both Has and Hyal genes and shifted hyaluronan toward a smaller size range.

291 Hyaluronan turnover is also increased.

292 o platelets previously adhered to sinusoidal hyaluronan via CD44.

293 When hyaluronan was combined with partially degraded, dansyl

294 conjugated hyaluronan, no internalization of hyaluronan was detected.

295 Hyaluronan was present in the smooth muscle cell layer s

296 H2 and N-acetyl moieties in the reacetylated hyaluronan were 0% and 98.7 +/- 1.5% respectively, where

297 whereas aggregates containing 15-s sonicated hyaluronan were internalized.

298 LTalpha also enhances the expression of hyaluronan which preferentially contributes to the recru

299 that FGFR activation induces accumulation of hyaluronan within the extracellular matrix and that bloc

300 reveal that Hyal-2 knockout mice accumulate hyaluronan within their bone marrow and within megakaryo