ライフサイエンスコーパス: vitronectin

1 in serum-free conditions (in the absence of vitronectin).

2 iated H1299 cell adhesion to fibronectin and vitronectin.

3 PAR increased cell adhesion and migration on vitronectin.

4 ind the arginine-glycine-aspartate domain of vitronectin.

5 adhesion by acting as a binding protein for vitronectin.

6 is occupied by its ligands, fibronectin and vitronectin.

7 creased adhesion of cells to fibronectin and vitronectin.

8 molecules of PAI-1 are capable of binding to vitronectin.

9 ll adhesion and spreading on fibronectin and vitronectin.

10 suggested a second PAI-1-binding site within vitronectin.

11 f PAI-1 in solution and its interaction with vitronectin.

12 the F-prostanoid receptor (FPS) to adhere to vitronectin.

13 ved for the binding of purified integrins to vitronectin.

14 e significantly increased by fibronectin and vitronectin.

15 with PAI-039 blocked the binding of PAI-1 to vitronectin.

16 e previously identified interaction site for vitronectin.

17 pping multiple substrate proteins, including vitronectin.

18 e sulfation sites in mouse lumican and human vitronectin.

19 of paxillin and p130Cas in cells adhering to vitronectin.

20 ng alpha(v)beta(3)-mediated cell adhesion to vitronectin.

21 essed the RGDfV-induced loss of spreading on vitronectin.

22 CD63 inhibits MC adhesion to fibronectin and vitronectin.

23 totactic migration towards the matrix factor vitronectin.

24 d increased adhesion to and migration toward vitronectin.

25 d and the active serpin forms complexes with vitronectin.

26 PAI-1 circulates in blood as a complex with vitronectin.

27 gate suspension or as monolayers adherent to vitronectin.

28 ed to both FGF-2 and fibrinogen but not with vitronectin.

29 ing abrogated upon plating of the cells onto vitronectin.

30 current clamp mode) occurred in response to vitronectin.

31 imilar voltages to I(h), was not affected by vitronectin.

32 ccal adhesin PspC and the human glycoprotein vitronectin.

33 I-1 binding to proteases and to its cofactor vitronectin.

34 ith the C-terminal heparin-binding domain of vitronectin.

35 lar matrix and integrin-mediated adhesion to vitronectin.

36 ral extracellular ligands, including uPA and vitronectin.

37 ace CEACAMs and to integrins, the latter via vitronectin.

38 lates the binding of uPAR to matrix-embedded vitronectin.

39 ng with integrin alphavbeta3 comparable with vitronectin.

40 inhibitor-1 (PAI-1), which is potentiated by vitronectin.

41 ivate PAI-1 in the presence of its cofactor, vitronectin.

42 ompounds inactivate PAI-1 in the presence of vitronectin.

43 5)-Cys(31) connectivity is present in native vitronectin; 2) only the native disulfide connectivity i

44 microg/mL), fibronectin (250 microg/mL), and vitronectin (33 microg/mL).

45 90% cleavage, clusterin (50%), ADAM9 (54%), vitronectin (54%), and alpha2-macroglobulin (55%), as we

46 SAXS) measurements were used to characterize vitronectin, a circulatory protein found in human plasma

47 sensitive ligands: the physiologic cofactor, vitronectin; a monoclonal antibody, 33B8, that binds pre

48 Vitronectin acquisition conferred serum resistance to bo

49 Elevated levels of TIMP3 and vitronectin, acting downstream of Notch3(ECD) deposition

50 + buffered by EGTA in the recording pipette, vitronectin-activated K+ current was abolished.

51 o the beta-propeller of alpha3beta1 empowers vitronectin adhesion by this integrin.

52 bent assay were used to measure fibronectin, vitronectin, alphaVbeta3 integrin, and IGF-I levels.

53 etal and adult beta-cells to collagen IV and vitronectin also results in the marked suppression of in

54 ated by vitronectin, we further propose that vitronectin alters the conformation of the RCL to allow

55 and apoptosis in HBMECs on poly-l-lysine or vitronectin, although cells detached only from vitronect

56 led a number of common factors, for example, vitronectin, an adhesion protein, dendritic cell-specifi

57 UTP also increased expression of vitronectin, an extracellular matrix protein that is a l

58 -ARs induced adhesion in three cell types to vitronectin, an interaction that was also integrin-, FGF

59 i-LIBS binding, but reduced cell adhesion to vitronectin and AP3.

60 igh-affinity alpha(v)beta(3) integrin ligand vitronectin and by antibodies to alpha(v)beta(3) integri

61 such as basic FGF, TGFbeta, fibronectin, and vitronectin and can serve as feeders for both autologous

62 tested only fibronectin and laminin but not vitronectin and collagen I stimulated trans-activation o

63 n expressed in Haemophilus influenzae, bound vitronectin and conferred serum resistance on this organ

64 of DsrA exhibited binding to fibronectin and vitronectin and conferred serum resistance to an H. ducr

65 as correlated with both increased binding of vitronectin and decreased binding of polymerized C9.

66 like pneumococcal surface protein, possesses vitronectin and factor H binding activity.

67 tween hTSP-1 and Hic differs from binding to vitronectin and factor H.

68 gands from the extracellular matrix ligands (vitronectin and fibronectin for alpha(v)beta(3) and alph

69 eractions via antibodies, exogenous ligands (vitronectin and fibronectin), and their RGD recognition

70 tal and adult beta-cells attached equally to vitronectin and integrin alpha(v)beta(5) was found to su

71 s, we found that whereas interaction between vitronectin and integrins diminished the ability of macr

72 reported, but also other ECM components like vitronectin and is an important regulator of cellular re

73 PAI-1 is inaccessible when PAI-1 is bound to vitronectin and may overlap with the PAI-1 vitronectin b

74 xtracellular matrix proteins fibronectin and vitronectin and mediates attachment of H. ducreyi to ker

75 ed alterations in adhesion and morphology on vitronectin and migration could be abolished by cultivat

76 B cells upregulate alphavbeta3 and adhere to vitronectin and milk-fat globule epidermal growth factor

77 econd, separate site for interaction between vitronectin and PAI-1.

78 MB) domain, mediates the interaction between vitronectin and plasminogen activator inhibitor 1 (PAI-1

79 Vitronectin and plasminogen activator inhibitor-1 (PAI-1

80 Vitronectin and plasminogen activator inhibitor-1 (PAI-1

81 We therefore hypothesized that IaI can bind vitronectin and promote vitronectin-induced epithelial r

82 exhibited migration and spreading defects on vitronectin and reduced sprouting in 3-dimensional fibri

83 integrin mediates adhesion to fibronectin or vitronectin and regulates various aspects of the inflamm

84 s with alpha(v)beta(3) upon cell adhesion to vitronectin and that this association requires beta(3) t

85 b-RPE deposits, such as complement factor H, vitronectin, and amyloid beta, revealed that HAP spherul

86 lation of the complement pathway (clusterin, vitronectin, and fibromodulin) and of amyloid deposition

87 IGF-I, vitronectin, and fibronectin RNA and protein levels were

88 es are able to bind to laminin, fibronectin, vitronectin, and hyaluronic acid, which are extracellula

89 were also observed to spread and migrate on vitronectin, and integrin alpha(v)beta(1) was found to b

90 ancer cell lines (C6, SNB75) on fibronectin, vitronectin, and laminin.

91 poietin-2 similarly to laminin, fibronectin, vitronectin, and more than to collagen-I, -III, and -IV.

92 actor beta-induced protein betaig-H3, DEL-1, vitronectin, and serine protease HtrA1 (P < 0.01).

93 PE binds plasminogen and also vitronectin, and the two human plasma proteins compete f

94 S1ED enhances alpha(v)beta(3) recognition of vitronectin; and treatments that target this domain, inc

95 TIMP3 and vitronectin are 2 extracellular matrix proteins that abn

96 lasminogen activator inhibitor-1 (PAI-1) and vitronectin are cofactors involved in pathological condi

97 igated whether increased levels of TIMP3 and vitronectin are responsible for aspects of CADASIL disea

98 es exclude proteolytic removal of PAI-1 from vitronectin as the mechanism, and show instead that cell

99 Our results demonstrate that PAI-1 and vitronectin assemble into higher order forms via a pathw

100 We show that IaI binds vitronectin at the arginine-glycine-aspartate site, ther

101 h Opc, Msf binds preferentially to activated vitronectin (aVn), engaging at its N-terminal region but

102 apoptotic vtn(-/-) neutrophils with purified vitronectin before intratracheal instillation decreased

103 ll adhesion, migration and signaling through vitronectin binding and interactions with integrins.

104 o vitronectin and may overlap with the PAI-1 vitronectin binding domain.

105 grins alpha5beta1 and alphavbeta6 and not on vitronectin binding integrins alphavbeta3 and alphavbeta

106 ncluded that neither fibronectin binding nor vitronectin binding is required for high-level serum res

107 The data imply that vitronectin binding may be an important strategy for the

108 Vitronectin binding required the R domains in the mature

109 inhibition by inactivators that bind at the vitronectin binding site.

110 -RGD constructs 10-13 inhibited biotinylated vitronectin binding to the purified alphaVbeta3 integrin

111 class II H. ducreyi strains mediated FN and vitronectin binding.

112 say, expression of alphavbeta3 integrin, and vitronectin binding.

113 23K/R101A variant demonstrated an even lower vitronectin-binding ability.

114 that possessed either intact antiprotease or vitronectin-binding activity to bleomycin-injured mice g

115 n resonance experiments demonstrated reduced vitronectin-binding affinity of the (Q123K) variant (K(D

116 We found that the vitronectin-binding capacity of PAI-1 was the primary de

117 The critical role of the vitronectin-binding function of PAI-1 in fibrosis was co

118 We conclude that the vitronectin-binding function of PAI-1 is necessary and s

119 at inhibits the generation of plasmin, and a vitronectin-binding function that interferes with cell a

120 A vitronectin-binding mutant of PAI-1 was equipotent with

121 In this study, we identified PspC as a vitronectin-binding protein interacting with the C-termi

122 PAR form, exposing the uPAR88-92 region, and vitronectin, both involved in fibrosis and in the fibrob

123 Finally, vitronectin bound to PspC was functionally active and in

124 on of PAI-1 by PAI-039 against free, but not vitronectin-bound PAI-1, suggesting for the first time a

125 d for pancreatic carcinoma cell migration on vitronectin but not on collagen.

126 ic ligands (urokinase plasminogen activator, vitronectin), but not via adjustment of the cholesterol

127 Preincubation of PAI-1 with vitronectin, but not bovine serum albumin, blocked PAI-0

128 induced transient loss of HBMEC spreading on vitronectin, but not their detachment, and induced apopt

129 These results indicate that binding of vitronectin by UspA2 is involved in the serum resistance

130 infection can be reduced by fibronectin and vitronectin, by down-regulation of integrin alphav, or b

131 g peptide RGDfV induces loss of spreading on vitronectin, cell detachment, and apoptosis.

132 dditional known drusen components, including vitronectin, clusterin, and serum amyloid P, thus sugges

133 We assessed five conditions and found that a vitronectin-coated substrate was the most efficient meth

134 o display a nonpolarized form of motility on vitronectin-coated substrates.

135 Using this new medium (E8) and vitronectin-coated surfaces, we demonstrate improved der

136 of endothelial cells cultured on Matrigel or vitronectin-coated surfaces.

137 concentration dependence of EPC adhesion (to vitronectin-, collagen type I-, fibronectin-, and lamini

138 e isolated, characterized, and cultured on a vitronectin/collagen scaffold and primed with SDF to gen

139 , the other 3 reactivity clusters (histones, vitronectin/collagen/chondroitin sulphate, and entactin/

140 xhibit reduced adhesion and migration toward vitronectin compared with wild-type cells.

141 Analytical ultracentrifugation on the PAI-1-vitronectin complex demonstrated that increasing NaCl co

142 This 2:1 PAI-1-vitronectin complex, with a sedimentation coefficient of

143 Cl concentration favors 1:1 versus 2:1 PAI-1-vitronectin complexes and hampers formation of higher or

144 We hypothesize that PAI-1-vitronectin complexes form in a stepwise and concentrati

145 model for the assembly of higher order PAI-1-vitronectin complexes via two distinct binding sites in

146 e were performed to identify different PAI-1-vitronectin complexes.

147 Vitronectin concentrations were significantly increased

148 erminal somatomedin B (SMB) domain of native vitronectin contains 44 amino acids, including a framewo

149 in (residues 1-44) of the human glycoprotein vitronectin contains the high-affinity binding sites for

150 psin, pancreatic polypeptide, complement C3, vitronectin, cortisol, AXL receptor kinase, interleukin-

151 at allows activation of proteins, among them vitronectin, critical for thrombus formation.

152 0 +/- 4.9 mV in naive neurones; P > 0.05) or vitronectin deficiency (-83.8 +/- 3.1 mV versus -82.0 +/

153 reduced in bronchoalveolar lavage fluid from vitronectin-deficient (vitronectin(-/-)) mice, as compar

154 ound in bronchoalveolar lavage obtained from vitronectin-deficient (vtn(-/-)) mice compared with wild

155 eurones in slices derived from wild-type and vitronectin-deficient mice.

156 These findings provide a novel vitronectin-dependent mechanism contributing to the deve

157 PAI-1 inhibition enhanced vitronectin-dependent transendothelial migration of huma

158 Furthermore, vitronectin-depleted NHS exhibited bactericidal activity

159 her, this work suggests that fibronectin and vitronectin deposition during demyelinating disease is a

160 a close relationship between fibronectin and vitronectin deposition, microglial activation, and micro

161 Furthermore, studying vitronectin-directed migration using (a) Fyn small inter

162 Plasma vitronectin does not bind to alphavbeta3 or alphaIIbbeta

163 this molecule does not modulate migration on vitronectin, does not associate with the major vitronect

164 leased PDI reduces disulfide bonds on plasma vitronectin, enabling vitronectin to bind to alphaVbeta3

165 vely larger contribution to total current in vitronectin-exposed cells contributing to the accelerati

166 ed differences in both G(max) and V(1/2): in vitronectin-exposed neurones there was a 35.4% increase

167 n rate of I(h) between neurones in naive and vitronectin-exposed slices (10 microg ml(-1) added to se

168 , HCN1 immunoreactivity appeared elevated in vitronectin-exposed slices, while HCN2 levels appeared u

169 n (V(1/2)) was not significantly affected by vitronectin exposure (-78.1 +/- 2.3 mV versus -80.0 +/-

170 Timp3 and vitronectin expression were genetically reduced in TgNot

171 proximately 1 nm) but does not interact with vitronectin, fibronectin, laminin, fibrinogen, and von W

172 is of endothelial cells cultured on gelatin, vitronectin, fibronectin, or laminin but not collagen ty

173 isulfide bonds in the SMB domain from native vitronectin forms a rigid core around the Cys(19): Cys(3

174 nhibits the binding of purified integrins to vitronectin; however, its inhibition of endothelial and

175 ithin the N-terminal somatomedin B domain of vitronectin; however, several studies have suggested a s

176 ition of the plasma proteins fibronectin and vitronectin in cerebral parenchyma.

177 n acute lung injury, we examined the role of vitronectin in LPS-induced pulmonary inflammation.

178 In contrast, haploinsufficiency or loss of vitronectin in TgNotch3(R169C) mice ameliorated white ma

179 cell, but not smooth muscle cell adhesion to vitronectin in the presence of PAI-1 requires both polym

180 l adhesion assembly reduces cell adhesion to vitronectin in the presence of PAI-1 to levels similar t

181 a significant increase in the expression of vitronectin in the retina of the experimental mice.

182 tronectin, although cells detached only from vitronectin, indicating that cell detachment was not req

183 Fura-2 microfluorimetry revealed that vitronectin induced a significant and sustained increase

184 n intracellular Ca2+ concentration, although vitronectin-induced Ca2+ current could not be detected.

185 ed that IaI can bind vitronectin and promote vitronectin-induced epithelial repair after injury.

186 of fetal beta-cells to both collagen IV and vitronectin induces significant glucose-independent insu

187 Collagen IV, but not vitronectin, induces comparable responses in adult beta-

188 prouting is known to involve the alphaVbeta3 vitronectin integrin on endothelium.

189 C molecules, did not interfere with the PspC-vitronectin interaction.

190 However, the factors that modify cell-vitronectin interactions after injury and help promote e

191 Vitronectin is a major ECM component that promotes epith

192 n of microglial activation by fibronectin or vitronectin is an important regulatory mechanism in vivo

193 dothelial and smooth muscle cell adhesion to vitronectin is at most 50-75%.

194 Vitronectin is present in large concentrations in serum

195 responses of adult and fetal beta-cells, and vitronectin is used as a substrate based on its unique p

196 nectin (Kd = 10.19 nM), but slightly less to vitronectin (Kd = 16.51 nM).

197 id residues of the human plasma glycoprotein vitronectin, known as the somatomedin B (SMB) domain, me

198 y of PAI-1 mutants to bind to the engineered vitronectin lacking the SMB domain.

199 In addition to fibrillin-1, fibronectin, vitronectin, laminin, and amyloid P-component, which are

200 he ECM protein, fibronectin, but adhesion to vitronectin, laminin, collagen-I, and collagen-IV was no

201 yptase epsilon could not cleave fibronectin, vitronectin, laminin, single-chain tissue-type plasminog

202 ited increased haptotaxis on fibronectin and vitronectin matrices that correlated with decreased adhe

203 nsity of 5 x 10(6) cells/cm(2) on a collagen/vitronectin matrix.

204 rhalis; this represents the first example of vitronectin-mediated serum resistance on a microbe.

205 ressor protein 4E-BP1, which is required for vitronectin-mediated tumor cell invasion.

206 nt (vitronectin(-/-)) mice, as compared with vitronectin(+/+) mice, after LPS exposure.

207 chemotaxis as compared with neutrophils from vitronectin(+/+) mice, and incubation of vitronectin(+/+

208 e concentrations were significantly lower in vitronectin(-/-) mice.

209 lar lavage fluid from vitronectin-deficient (vitronectin(-/-)) mice, as compared with vitronectin(+/+

210 To investigate this secondary site, a vitronectin mutant lacking the somatomedin B domain (rDe

211 -2, and IL-1beta after LPS exposure than did vitronectin(+/+) neutrophils and also showed greater deg

212 rom vitronectin(+/+) mice, and incubation of vitronectin(+/+) neutrophils with vitronectin was associ

213 lear accumulation of NF-kappaB compared with vitronectin(+/+) neutrophils.

214 Vitronectin(-/-) neutrophils consistently produced more

215 Vitronectin(-/-) neutrophils demonstrated decreased KC-i

216 not secreting endogenous FN (suppressive if vitronectin, non-suppressive but non-supportive if III(7

217 s demonstrate that the inhibitory effects of vitronectin on efferocytosis involve interactions with b

218 und specifically to fibronectin (Fn) but not vitronectin or collagens.

219 However, cells maximally spread on vitronectin or fibronectin still responded to the fibron

220 35 human mammary carcinoma cell spreading on vitronectin or S1-specific antibody.

221 lls expressing gB and gHgL can be blocked by vitronectin or triggered by addition of soluble truncate

222 1 collagen matrices, but not to fibronectin, vitronectin, or laminin, demonstrated a significant incr

223 alpha-helices D and E in PAI-1 and a site in vitronectin outside of the SMB domain.

224 ea that may promote assembly of higher order vitronectin-PAI-1 complexes.

225 tion using a surface plasmon resonance based vitronectin-PAI-1-SMB competition assay allowed us to co

226 In addition, using vitronectin peptides to block Msf-aVn interactions, aVn-

227 Using a series of vitronectin peptides, the C-terminal heparin-binding dom

228 Deposits were rich in vitronectin, photoreceptor-associated proteins, and Iba1

229 eta3 with extracellular matrix ligands (e.g. vitronectin) plays a critical role in insulin-like growt

230 le, immobilized, as well as cellularly bound vitronectin possesses different conformations.

231 isulfide topology in the SMB domain of human vitronectin, providing biochemical as well as functional

232 segment of 51 amino acid residues of intact vitronectin purified from human blood.

233 thrombus generation in mice demonstrate that vitronectin rapidly accumulates on the endothelium and t

234 The role of the vitronectin receptor (alpha(v)beta(3)-integrin) as a tum

235 osphatidylserine (PS)-exposing cells and the vitronectin receptor (VR) on phagocytes.

236 Therefore, the vitronectin receptor might not be an appropriate therape

237 pidermal growth factor-8, and its microglial vitronectin receptor was sufficient to rescue up to 90%

238 tronectin, does not associate with the major vitronectin receptor, alpha(v)beta(3) integrin, and does

239 own about kindlin regulation of the related "vitronectin receptor," alphaVbeta3.

240 in polymerization) or cyclo(RGDfV) (to block vitronectin receptors) significantly prevented neuronal

241 Among the two vitronectin receptors, alphavbeta3 and alphavbeta5 integ

242 nificantly reduced binding to fibrinogen and vitronectin, relative to non-risk, both in purified prot

243 immobilized integrins, using fibronectin and vitronectin, respectively, as competitors.

244 ter understanding of the domain structure of vitronectin resulted from low-resolution models develope

245 -mediated adhesion of hematopoietic cells to vitronectin results in activation of the Rho GTPases.

246 domain demonstrates that this mutant form of vitronectin retains PAI-1 binding.

247 ite that is located directly adjacent to the vitronectin RGD integrin binding sequence.

248 The plasma adhesion proteins fibronectin and vitronectin serve as cofactors for these three antiangio

249 The somatomedin B domain of vitronectin (SMBD) did not affect SI for any proteinase

250 The binding of PAI-1 to vitronectin sterically blocks integrin access to this si

251 We suggest that vitronectin-stimulated increases in I(h) may potentially

252 aging the extracellular matrix (ECM) protein vitronectin, strongly upregulate both mTOR activity and

253 and facilitates the migration of cells on a vitronectin substrate by regulating alpha v integrin cel

254 Binding experiments with immobilized vitronectin suggested a region N-terminal to the identif

255 ascular endothelial cells (HBMECs) plated on vitronectin, suggesting that sphingomyelin hydrolysis co

256 hese same three wild-type strains bound more vitronectin than did their uspA2 mutants.

257 in 35000HP bound more C4 binding protein and vitronectin than FX517 but not factor H.

258 Pneumococci engage vitronectin, the human adhesive glycoprotein and complem

259 g the first 51 amino acids from human plasma vitronectin, the somatomedin B (SMB) domain, has been de

260 ulfide bonds on plasma vitronectin, enabling vitronectin to bind to alphaVbeta3 and alphaIIbbeta3.

261 saturation of the two PAI-1-binding sites of vitronectin to form the 2:1 complex.

262 ly, we have shown that Nm Opc binds to serum vitronectin to inhibit complement-mediated killing.

263 and alpha(v)beta(5) engagement with adsorbed vitronectin to promote colony formation.

264 etory IgA competitively inhibited binding of vitronectin to purified PspC and to PspC-expressing pneu

265 -I, whereas addition of the active region of vitronectin to RECs grown in normal glucose enhanced the

266 Binding of vitronectin to the complexes of NBD P9 PAI-1 with mAbs r

267 tant wild-type strains; addition of purified vitronectin to this serum restored serum resistance.

268 hich comprises the N-terminal 44 residues of vitronectin, to the flexible joint region of PAI-1, incl

269 tion of luminal alpha(v)beta(3) receptors by vitronectin triggers Ca2+ influx.

270 gher on fibronectin and VCAM-1 compared with vitronectin, types I or IV collagen.

271 ted chemotaxis, Rac and Vav2 activation, and vitronectin up-regulation were inhibited by pretreatment

272 s (fibronectin, types I and IV collagen, and vitronectin), vascular cell adhesion molecule (VCAM)-1,

273 s that bind beta3 integrins (fibronectin and vitronectin) versus substrates that only bind beta1 inte

274 demonstrate meningococcal interactions with vitronectin via a novel adhesin, Msf (meningococcal surf

275 The high-affinity binding site in human vitronectin (VN) for plasminogen activator inhibitor-1 (

276 en uPAR and the extracellular matrix protein vitronectin (VN) for the signaling activity of the recep

277 Vitronectin (VN) in provisional extracellular matrix (EC

278 leavage of ECM proteins fibronectin (FN) and vitronectin (Vn) into small fragments and increased bind

279 , we revealed that PH is also a receptor for vitronectin (Vn), an abundant plasma protein that regula

280 lasts (HCFs) were grown on fibronectin (FN), vitronectin (VN), or collagen (CL) in supplemented serum

281 en identified previously as a staphylococcal vitronectin (Vn)-binding protein.

282 ubation of vitronectin(+/+) neutrophils with vitronectin was associated with increased chemotaxis.

283 Adhesion to fibronectin, collagens, and vitronectin was compromised.

284 ation was also noted: macrophage adhesion to vitronectin was enhanced by uPA and blocked by plasminog

285 The SMB domain of vitronectin was isolated by digesting the protein with e

286 showed that the influence of fibronectin and vitronectin was mediated by the alpha(5)beta(1) and alph

287 entation of the extracellular matrix protein vitronectin, we accomplished reversible differentiation

288 king peptides into wtPAI-1 is accelerated by vitronectin, we further propose that vitronectin alters

289 itro is strongly promoted by fibronectin and vitronectin, we set out to examine the possibility that

290 ation, total brain levels of fibronectin and vitronectin were strongly increased and there was a clos

291 , we found that SEMA3F decreased adhesion to vitronectin, whereas integrin-linked kinase (ILK) kinase

292 adhesion to the extracellular matrix protein vitronectin, which is a naturally occurring ligand for a

293 Because PAI-1 binds vitronectin with approximately 10-100-fold higher affini

294 ype-1 (PAI-1), binds to the adhesion protein vitronectin with high affinity at a site that is located

295 Interaction of vitronectin with integrin alphavbeta3 results in the con

296 Preincubation of vitronectin with plasminogen activator inhibitor-1 elimi

297 be essential for the interaction of soluble vitronectin with PspC.

298 in and C-terminal heparin-binding domains of vitronectin with respect to the N-terminal somatomedin B

299 ingest apoptotic cells, interaction between vitronectin with urokinase-type plasminogen activator re

300 nt amplitude was preferentially sensitive to vitronectin, with its relatively larger contribution to