ライフサイエンスコーパス: Willebrand

1 Thirty-six Bretoncelles-Meishan-Willebrand pigs of either gender.

2 se (VWD) with VWF levels </=30 U/dL from the Willebrand in The Netherlands (WiN) study using the VWFp

3 2, and 3 von Willebrand disease (VWD) in the Willebrand in the Netherlands (WiN) study by using the r

4 Von Willebrand disease (VWD) is an inherited bleeding disord

5 Von Willebrand disease (VWD) is the most common inherited bl

6 von Willebrand disease (VWD) is the most common inherited bl

7 Von Willebrand disease (VWD) type 2B is characterized by mut

8 Von Willebrand factor (VWF) contains binding sites for plate

9 von Willebrand factor (VWF) has been considered as a marker

10 Von Willebrand factor (vWF) is a biomarker of endothelial dy

11 Von Willebrand factor (VWF) is a key hemostatic protein synt

12 von Willebrand factor (VWF) is a large multimeric glycoprote

13 Von Willebrand factor (VWF) is a multimeric plasma glycoprot

14 Von Willebrand Factor (VWF) is a multimeric protein crucial

15 von Willebrand factor (VWF) is a particularly intriguing cas

16 von Willebrand factor (VWF) is amongst others synthesized by

17 von Willebrand Factor (VWF) is an ultralong, concatameric, a

18 von Willebrand factor (VWF) laboratory testing and full-leng

19 Von Willebrand factor (VWF) multimer size is controlled thro

20 Von Willebrand factor (VWF) plays a central role in hemostas

21 von Willebrand factor (vWF) secretion by endothelial cells (

22 von Willebrand factor (VWF) strings are removed from the end

23 Von Willebrand factor (VWF), a key player in hemostasis, is

24 von Willebrand factor (VWF), a multimeric protein with a cen

25 Von Willebrand factor is proposed to be mechanically activat

26 von Willebrand factor multimers were abnormal in 1 of 26 nor

27 Von Willebrand factor, an ultralarge concatemeric blood prot

28 32 subjects with type 3 or severe type 1 von Willebrand disease (VWD) in a prospective phase 1, multi

29 1 participants (318 patients with type 1 von Willebrand disease [VWD] and 173 unaffected family membe

30 actor (VWF) gene in a family with type 1 von Willebrand disease.

31 EDE levels of VCAM-1, von Willebrand factor, platelet-derived growth factor (PDGF)

32 n D-dimer by 24% (95% CI, -30% to -18%), von Willebrand factor by 22% (95% CI, -35% to -9%), thrombin

33 Type 2 von Willebrand disease (VWD) includes a wide range of qualit

34 helial injury, including angiopoietin-2, von Willebrand Factor, and soluble thrombomodulin.

35 Mutations causing type 2B von Willebrand disease (VWD), platelet-type VWD (PT-VWD), an

36 In type 2M von Willebrand disease, two rare mutations (G1324A and G1324

37 ecreased FVIII binding affinity (type 2N von Willebrand disease [VWD]).

38 ted the pathologic mechanism acting in 3 von Willebrand disease (VWD) families with putative splicing

39 the pathophysiology of types 1, 2, and 3 von Willebrand disease (VWD) in the Willebrand in the Nether

40 ogy of 658 patients with type 1, 2, or 3 von Willebrand disease (VWD) with VWF levels </=30 U/dL from

41 of 16%, factor IX (FIX) activity of 74%, von Willebrand factor (VWF) activity of 12%, VWF antigen act

42 With a von Willebrand factor A (VWA) domain and six thrombospondin

43 ing with AAA+ ATPase (ViaA) containing a von Willebrand Factor A domain.

44 As both integrins and MUC5AC have a von Willebrand factor domain, we assessed for possible inter

45 We investigated a case of acquired von Willebrand syndrome (AVWS) secondary to a nonneutralizin

46 t VWF multimers consistent with acquired von Willebrand syndrome (AVWS).

47 plantation, leading to the term acquired von Willebrand syndrome (AVWS).

48 display a condition similar to acquired von Willebrand syndrome, exhibiting significantly less high

49 rotein) and endothelial cell activation (von Willebrand factor) both at baseline and during follow-up

50 assigns this association to the ADAMTS13 von Willebrand factor-binding domain (P=1.2x10(-4)).

51 he development of alloantibodies against von Willebrand factor (VWF) represents a rare but serious co

52 tative VWF deficiencies in the blood and von Willebrand disease.

53 such as hemophilia A, hemophilia B, and von Willebrand disease.

54 cation end products (3.5 [1.7-7.2]), and von Willebrand Factor (3.1 [2.0-5.2]).

55 n collagenous extracellular matrices and von Willebrand factor (VWF) are critical for hemostasis and

56 d that bind to putative phospholipid and von Willebrand factor (VWF) binding epitopes and block endoc

57 Plasma factor VIII (FVIII) and von Willebrand factor (VWF) circulate together as a complex.

58 gainst complement C1q (Fab anti-C1q) and von Willebrand factor (VWF) led us to investigate a potentia

59 We investigated whether platelets and von Willebrand factor (VWF) mediate bacterial adhesion to th

60 rogressed through Rab4(+), Rab11(+), and von Willebrand factor (VWF)(+) compartments in wild-type pla

61 eraction between factor VIII (FVIII) and von Willebrand factor (VWF).

62 otein tyrosine phosphatase (VE-PTP), and von Willebrand factor (vWf).

63 ry requires both factor VIII (FVIII) and von Willebrand factor (VWF).

64 r inhibitor type 1 [PAI-1], D-dimer, and von Willebrand factor [vWF]) were measured in plasma.

65 Increase in fibrinogen, factor VIII, and von Willebrand factor and decrease in antithrombin III corre

66 postoperative portal venous pressure and von Willebrand factor antigen levels as a marker for intrahe

67 ts (IsdA and IsdB), coagulase (Coa), and von Willebrand factor binding protein (vWbp)-are dispensable

68 r the <1st eGFR percentile category) and von Willebrand factor levels (adjusted mean difference, 60 I

69 via concurrently raised factor VIII and von Willebrand factor levels.

70 mbinant ADAMTS13 eliminated platelet and von Willebrand factor molecular imaging signal.

71 deposited diffusely on capillaries, and von Willebrand factor released from endothelial cells coated

72 rowth factor-binding protein (IGFBP) and von Willebrand factor type C (vWC) domains.

73 type VI, alpha-3; thrombospondin 2; and von Willebrand factor) were verified by real-time polymerase

74 apolipoprotein A-I, thrombomodulin, and von Willebrand factor, may contribute to vascular disease an

75 Angiopoietin-2 and von Willebrand factor, which are biomarkers of endothelial a

76 tes the coagulases staphylocoagulase and von Willebrand factor-binding protein, both of which form a

77 ue inhibitor of metalloproteinase 2, and von Willebrand factor-in plasma samples from 611 patients.

78 nly at the ABO locus for factor VIII and von Willebrand factor.

79 n controls, most notably factor VIII and von Willebrand factor.

80 nd apoptosis (release of fractalkine and von Willebrand factor; increased caspase 3 expression).

81 VWS) secondary to a nonneutralizing anti-von Willebrand factor (VWF) antibody associated with an auto

82 Caplacizumab, an anti-von Willebrand factor humanized single-variable-domain immun

83 type 1 motif, member 13), also known as von Willebrand factor (VWF)-cleaving protease, as a protecti

84 mponents of the thrombus itself, such as von Willebrand factor, fibrinogen, and thrombocytes.

85 We therefore aimed to assess von Willebrand factor (vWF), a marker of endothelial damage,

86 We assessed von Willebrand factor (VWF), factor VIII, platelet activatio

87 ctions, increased endothelial-associated von Willebrand factor, particularly in a multimerized form,

88 4), through which hyperglycemia augments von Willebrand factor (VWF) expression and secretion.

89 evels of amyloid-beta40, amyloid-beta42, von Willebrand factor (VWF; a measure of microvascular densi

90 The ratios between von Willebrand factor propeptide (VWFpp) or factor VIII acti

91 no-regulation of receptor-ligand binding.Von Willebrand factor (VWF) is a blood protein involved in c

92 The blood von Willebrand factor (VWF) mediates platelet adhesion to in

93 , and rs505922 in the ABO gene with both von Willebrand factor (p = 4.7 x 10(-57)) and factor VIII (p

94 lebrand factor-platelet strings (on both von Willebrand factor and platelets) and on endothelial cell

95 e, which in gnathostomes is regulated by von Willebrand factor (VWF), a glycoprotein that mediates th

96 platelet adhesion, which is mediated by von Willebrand factor (VWF).

97 amine-evoked secretion of the WPB cargos von Willebrand factor and P-selectin.

98 and factor VIII (FVIII) and its carrier von Willebrand factor (vWF) play key roles in hemostasis.

99 To evaluate vascular cells, von Willebrand factor (vWF) and vascular endothelial growth

100 iver, and its main function is to cleave von Willebrand factor (VWF) anchored on the endothelial surf

101 thrombotic properties because it cleaves von Willebrand factor (VWF) in smaller, less active multimer

102 The metalloprotease ADAMTS13 cleaves von Willebrand factor (VWF) within endovascular platelet agg

103 ADAMTS13 metalloprotease cleaves von Willebrand factor (VWF), thereby inhibiting platelet agg

104 e for such a key component as it cleaves von Willebrand factor multimers, reduces platelet adhesion a

105 ombospondin motifs 13 (ADAMTS13) cleaves von Willebrand factor, reducing its prothrombotic activity.

106 nt human ADAMTS13 (rhADAMTS13), cleaving von Willebrand factor (VWF), reduces leukocyte recruitment i

107 regulates blood coagulation by cleaving von Willebrand factor (VWF), reducing its procoagulant activ

108 ssociated peptide, TGF-beta1, clusterin, von Willebrand factor, multimerin-1, protein disulfide isome

109 th plasma-derived factor VIII containing von Willebrand factor had a lower incidence of inhibitors th

110 th plasma-derived factor VIII containing von Willebrand factor or recombinant factor VIII.

111 ata showing the role of platelet-derived von Willebrand factor (VWF) in mediating ischemic stroke inj

112 Replacement therapy with plasma-derived von Willebrand factor-factor VIII concentrates represents th

113 t growth factor-2), thrombosis (D-dimer, von Willebrand factor, thrombin-antithrombin III), inflammat

114 ed with the bleeding diathesis disorder, von Willebrand disease (vWD), on the structure and rheology

115 ause the common human bleeding disorder, von Willebrand disease (VWD).

116 ctions are in part caused by endothelial von Willebrand factor large multimers, which can be reversed

117 l tubular cytokeratin 7, and endothelial von Willebrand factor markers.

118 Enhanced von Willebrand factor (VWF) clearance is important in the et

119 of terminal sialic acid causes enhanced von Willebrand factor (VWF) clearance through the Ashwell-Mo

120 eposition was independent of fibrinogen, von Willebrand factor, beta3 integrin, and platelets.

121 The structure reveals the basis for von Willebrand disease phenotypes and the fold and disulfide

122 The patients' sera were tested for von Willebrand factor (VWF) antigen, VWF collagen-binding ac

123 ar techniques to dissect a mechanism for von Willebrand factor (vWF) secretion from endothelial cells

124 ed to have a higher binding affinity for von Willebrand factor (VWF).

125 affinity, dependence on separation from von Willebrand factor, and mediation by the C2 domain.

126 ow that the endothelial-restricted gene, von Willebrand factor (VWF), is expressed in a mosaic patter

127 The large multimeric glycoprotein von Willebrand Factor (VWF) plays a pivotal adhesive role du

128 The large plasma glycoprotein von Willebrand factor (VWF) senses hydrodynamic forces in th

129 revented by the multidomain glycoprotein von Willebrand factor (VWF), which binds exposed collagen at

130 arterial lumen is mediated by GpIbalpha-von Willebrand Factor (VWF) interactions.

131 diastolic blood pressures), hemostasis (von Willebrand factor, soluble CD40 ligand, and P-selectin),

132 The primary hemostatic von Willebrand factor (vWF) functions to sequester platelets

133 e I enhancer binding protein 1 (HIVEP1), von Willebrand factor (VWF), glutathione peroxidase 3 (GPX3)

134 However, von Willebrand factor (VWF), with help from our circulatory

135 predicts the risk of future bleeding in von Willebrand disease (VWD) patients.

136 or qualitative defects in VWF result in von Willebrand disease (VWD), a common inherited bleeding di

137 Mutations in VWF in von Willebrand disease contribute to and are illuminated by

138 minal cystine knot (CK) (CTCK) domain in von Willebrand factor (VWF) mediates dimerization of proVWF

139 anemia, associated with a deficiency in von Willebrand factor (VWF)-cleaving protease ADAMTS13.

140 defect is not related to alterations in von Willebrand factor (VWF)-GPIb adhesive function or platel

141 e results demonstrate that variations in von Willebrand factor multimeric pattern are highly dynamic,

142 cell and junctional proteins, including von Willebrand factor, CD31, occludin, and vascular endothel

143 sion of endothelial cell genes including von Willebrand factor, VE-cadherin, and eNOS were observed w

144 ical outcomes in patients with inherited von Willebrand disease (VWD).

145 s synthesize both the clotting initiator von Willebrand factor (VWF) and the complement regulator fac

146 king during arterial thrombosis involves von Willebrand Factor (VWF) multimers.

147 Unusually large von Willebrand factor (VWF), the first responder to vascular

148 Here we show that binding of its ligand, von Willebrand factor, under physiological shear stress indu

149 tor XIII (FXIIIa) covalently cross-links von Willebrand factor (VWF) to polymerizing fibrin.

150 coefficient adjusted for log age and log von Willebrand factor (VWF) antigen was -0.32 (P = .004), ac

151 osis and management of patients with low von Willebrand factor (VWF) levels (30-50 IU/dL).

152 acellular proteins, among which are many von Willebrand factor C (vWC) domain-containing proteins.

153 , P < 0.01) or endothelial injury marker von Willebrand factor (R = +0.3; P < 0.01).

154 her with that of the endothelial marker, von Willebrand factor, in human and rat liver tissue, at adv

155 ly folded and mutation-induced misfolded von Willebrand disease (VWD) variants, we test a recently pr

156 Multimeric von Willebrand factor (VWF) is essential for primary hemosta

157 edge, this is the first reported case of von Willebrand deficiency corrected through lung transplanta

158 The diagnosis of von Willebrand disease (VWD) is complicated by issues with c

159 but serious complication of treatment of von Willebrand disease (VWD), occurring in ~5% to 10% of typ

160 eavage process, cause a distinct form of von Willebrand disease (VWD), VWD type 2A.

161 ols and subjects with different types of von Willebrand disease (VWD).

162 ctivation, and on the pathophysiology of von Willebrand disease and related thrombocytopenic disorder

163 or the Molecular and Clinical Biology of von Willebrand Disease with type 2 VWD.

164 us gain insight into the pathogenesis of von Willebrand disease, design alternative treatment options

165 learance is important in the etiology of von Willebrand disease.

166 New options for laboratory assessment of von Willebrand factor (VWF) activity include a new platelet-

167 support causes pathologic degradation of von Willebrand factor (vWF) and bleeding from gastrointestin

168 We identify reduced plasma levels of von Willebrand factor (VWF) and reduced VWF synthesis, speci

169 y increased accumulation and activity of von Willebrand factor (vWF) at poststenotic sites.

170 trophils inhibit proteolytic cleavage of von Willebrand factor (VWF) by ADAMTS13 in a concentration-d

171 platelet GPIbalpha adhesive A1 domain of von Willebrand factor (VWF) causes quantitative VWF deficien

172 hobic pocket in the central A2 domain of von Willebrand factor (VWF) for its proteolysis.

173 hrough JAK2V617F-regulated inhibition of von Willebrand factor (VWF) function and/or secretion.

174 Approximately 10% of von Willebrand factor (VWF) gene mutations are thought to al

175 Although much of the function of von Willebrand factor (VWF) has been revealed, detailed insi

176 An elevated level of von Willebrand factor (VWF) in diabetic patients is associat

177 as been associated with plasma levels of von Willebrand factor (VWF) in healthy individuals.

178 et al have extended our understanding of von Willebrand factor (VWF) in the pathogenesis of malaria.

179 atients and found a distinct presence of von Willebrand factor (VWF) in various samples.

180 Activation by elongational flow of von Willebrand factor (VWF) is critical for primary hemostas

181 lycoprotein Ibalpha and the A1 domain of von Willebrand factor (VWF) mediates tethering/translocation

182 Association with the D'D3 domain of von Willebrand factor (VWF) stabilizes factor VIII (FVIII) i

183 081, a Nanobody against the A1 domain of von Willebrand factor (VWF) that blocks VWF binding to GPIb,

184 The ability of von Willebrand factor (VWF) to initiate platelet adhesion de

185 by mutations causing enhanced binding of von Willebrand factor (VWF) to platelets.

186 e that cleaves large multimeric forms of von Willebrand factor (VWF) to smaller, less adhesive forms.

187 ulability by affecting the production of von Willebrand factor (vWF), a key initiator of the clotting

188 the size of nanostructures ("quanta") of von Willebrand factor (vWF), the main WPB cargo.

189 downregulation inhibits the secretion of von Willebrand factor (VWF), the most abundant cargo in WPBs

190 uring posttranslational modifications of von Willebrand factor (VWF), the VWF propeptide (VWFpp) is c

191 patients with SIRS and plasma levels of von Willebrand factor (VWF), thrombospondin-1, myeloperoxida

192 lates the platelet-tethering function of von Willebrand factor (VWF).

193 initial platelet adhesion in absence of von Willebrand factor (VWF).

194 nge in the platelet-binding A1 domain of von Willebrand factor (VWF).

195 of normal ADAMTS-13-mediated cleavage of von Willebrand factor (VWF).

196 wth of microthrombi that are composed of von Willebrand factor and platelets, which account for the t

197 Basal plasma levels of von Willebrand factor and recruitment of platelets to the in

198 high molecular weight (HMW) multimers of von Willebrand factor defect could be instantaneous after ac

199 icrobubbles targeted to the A1 domain of von Willebrand factor demonstrated selective signal enhancem

200 The content of von Willebrand factor in the products and switching among pr

201 nhibitor development, and the content of von Willebrand factor in the products and switching among pr

202 Re-compaction of Von Willebrand factor is accelerated by intramolecular inter

203 high-molecular-weight (HMW) multimers of von Willebrand factor or point-of-care assessment of hemosta

204 lands (WiN) study by using the ratios of von Willebrand factor propeptide (VWFpp) or factor VIII acti

205 de range of qualitative abnormalities of von Willebrand factor structure and function resulting in a

206 -serum medium showed robust secretion of von Willebrand factor when stimulated with various agonists.

207 With the exception of von Willebrand factor, all the above changes correlated sign

208 With the exception of von Willebrand factor, assessed with the median cutoff metho

209 let buds containing incorrect numbers of von Willebrand factor-positive granules.

210 signal as they tether and translocate on von Willebrand factor (VWF) of injured arterial surfaces aga

211 rongly affects firm platelet adhesion on von Willebrand factor (VWF) under arterial flow.

212 m, under shear, induced C3 deposition on von Willebrand factor-platelet strings (on both von Willebra

213 nemia, thalassemia, or hemophilia A/B or von Willebrand disease were enrolled at 31 study sites in th

214 beta-thalassemia, and hemophilia A/B or von Willebrand disease, respectively.

215 therapy with desmopressin (DDAVP) and/or von Willebrand factor (VWF)/factor VIII concentrates.

216 Adjustment for factor VIII or von Willebrand factor attenuated these odds ratios, indicati

217 This mechanism may apply to other von Willebrand factor A domains undergoing large conformatio

218 with an early marked increase in plasma von Willebrand factor (VWF) levels, together with a patholog

219 with von Willebrand disease pigs, plasma von Willebrand factor (vWF) was significantly increased afte

220 rol levels (HDL-C and LDL-C), and plasma von Willebrand factor (vWF).

221 tion of the vascular endothelium (plasma von Willebrand levels) and the fibrinolytic system (plasma t

222 Ib-IX complex, which binds to plasmatic von Willebrand factor adsorbed on laminins.

223 Platelet-von Willebrand factor (VWF) interactions must be tightly reg

224 Platelet-von Willebrand factor (VWF) is stored within alpha-granules

225 alence approaching 1% of the population, von Willebrand disease (vWD) is the most common hereditary b

226 5416 mouse model identified the presence von Willebrand factor/alpha-smooth muscle actin-positive end

227 by the acute release of the procoagulant von Willebrand factor, which is stored in unique secretory g

228 dial infarction, mediated by a prolonged von Willebrand plasma half life leading to thrombosis.

229 s), which contain the hemostatic protein von Willebrand factor (VWF) and a cocktail of angiogenic and

230 hrough its binding to the plasma protein von Willebrand factor (VWF) and transmits a signal into the

231 the multimeric blood coagulation protein von Willebrand Factor (VWF) by ADAMTS13 is crucial for preve

232 ations in the ultralong vascular protein von Willebrand factor (VWF) cause the common human bleeding

233 The plasma protein von Willebrand factor (VWF) is essential for hemostasis init

234 he release of the procoagulatory protein von Willebrand factor (VWF) is essential for malignancy, the

235 major component, the hemostatic protein von Willebrand factor (VWF), is known to assemble into long

236 s observed in the alpha-granule proteins von Willebrand factor and P-selectin.

237 n (GP) Ib-IX-V complex, which recognizes von Willebrand factor (VWF) in the matrix.

238 and pharmacokinetics (PK) of recombinant von Willebrand factor (rVWF) combined at a fixed ratio with

239 3 clinical trial evaluating recombinant von Willebrand factor (rVWF) for the treatment of hemorrhagi

240 and hemostatic efficacy of a recombinant von Willebrand factor (rVWF) for treatment of bleeds in seve

241 S13) is a metalloprotease that regulates von Willebrand factor (VWF) function.

242 rotein Ib-IX-V with endothelial-released von Willebrand factor with a supporting role for the P-selec

243 lood vessels under shear stress requires von Willebrand factor (VWF).

244 , we simultaneously monitored reversible Von Willebrand factor extension and binding to GPIbalpha und

245 is the capacity of endothelial-secreted von Willebrand factor (VWF) to assemble into thick bundles o

246 ockade of adhesion molecules P-selectin, von Willebrand factor (VWF), E-selectin, vascular cell adhes

247 atients with severe CAV had raised serum von Willebrand factor and decreased serum thrombomodulin.

248 (rVWF) for treatment of bleeds in severe von Willebrand disease (VWD).

249 type 1 repeats, member 13), the specific von Willebrand factor-cleaving protease.

250 Endothelial cells store von Willebrand Factor (vWF), a glycoprotein essential to hae

251 domains of integrin are the best-studied von Willebrand factor A domains undergoing significant confo

252 th its binding to phospholipid surfaces, von Willebrand factor, or other components of the intrinsic

253 ng domains of carbonic anhydrase, Sushi, Von Willebrand factor type A, and chitin binding, were ident

254 prevalence of acquired vWD (often termed von Willebrand syndrome or vWS) is now believed to be signif

255 actors bind to both an N- and C-terminal von Willebrand factor C domain of chordin.

256 emperature and force the hypothesis that von Willebrand disease mutations disrupt A2 force sensing by

257 Limited data suggest that von Willebrand factor (VWF) abnormalities may accompany the

258 We discovered that von Willebrand factor (VWF) acts as a cofactor for factor I-

259 ate in vitro and in an animal model that von Willebrand factor (VWF) self-association under shear str

260 We show that Von Willebrand factor is activated through a two-step confor

261 e focus on emerging data suggesting that von Willebrand factor, coagulation cascade activation, and d

262 The von Willebrand factor (VWF) A1 and A3 domains are structural

263 igger a conformational transition in the von Willebrand factor (VWF) A2 domain, from its native folde

264 Rare missense mutations in the von Willebrand factor (VWF) A3 domain that disrupt collagen

265 stage of hemostasis and thrombosis: the von Willebrand factor (VWF) binding to platelet glycoprotein

266 is characterized by a deficiency of the von Willebrand factor (VWF) cleaving enzyme, ADAMTS13 (a dis

267 Binding to the von Willebrand factor (VWF) D'D3 domains protects factor VII

268 t mutation, c.7464C>T, in exon 44 of the von Willebrand factor (VWF) gene in a family with type 1 von

269 e (VWD) have a qualitative defect of the von Willebrand factor (VWF) protein activities.

270 In most patients, the von Willebrand factor (VWF) rapidly loses large multimers an

271 platelet activation induced through the von Willebrand Factor (VWF) receptor, the glycoprotein Ib-IX

272 The von Willebrand factor (VWF) synthesized and secreted by endo

273 caused by the functional changes of the von Willebrand Factor (VWF), which mediates coagulation of b

274 humoral autoimmune response against the von Willebrand factor A domain-containing protein 5a, an ext

275 the co-injection of mRNA coding for the von Willebrand factor C domain of collagen IIalpha1a, indica

276 or complex GPVI-FcR gamma-chain, and the von Willebrand factor receptor complex GPIb-IX-V, which are

277 Here we demonstrate that the von Willebrand factor type A (VWA) domain within the cleaved

278 ce similarity that TSP-1 shares with the von Willebrand type C domain of Crossveinless 2 (CV-2), a BM

279 We also report that the von Willebrand type C domain of TSP-1 is likely responsible

280 Binding to von Willebrand factor (VWF) was maintained for all conjugate

281 GPIbalpha, impaired platelet adhesion to von Willebrand factor, and inability to form stable thrombi.

282 ogical shear forces in the blood trigger von Willebrand factor (VWF) unfolding which exposes the Y160

283 at expression or infusion of a truncated von Willebrand factor (VWF) fragment containing the factor V

284 ibits the interaction between ultralarge von Willebrand factor multimers and platelets.

285 no aHUS patients demonstrated ultralarge von Willebrand factor multimers at presentation.

286 y aggregation of platelets on ultralarge von Willebrand factor multimers.

287 ic mimicry (VM), the mature vasculature (von Willebrand Factor) and tumor induced angiogenesis (by me

288 remain anchored to the vascular wall via von Willebrand factor and reveal significant neutrophil elas

289 D45) and endothelial markers (CD31, vWf, von Willebrand factor).

290 ased proportion of high-molecular-weight von Willebrand factor multimers could reduce platelet adhesi

291 te character coincide with regions where Von Willebrand disease mutations induce misfolded molten glo

292 pproximately 20% to 25% of patients with von Willebrand disease (VWD) have a qualitative defect of th

293 hemorrhagic events in all patients with von Willebrand disease (VWD).

294 In experimental models with von Willebrand disease pigs, plasma von Willebrand factor (v

295 these and other VWF coding variants with von Willebrand factor (VWF) and factor VIII (FVIII) levels i

296 vWbp has been reported to associate with von Willebrand factor and fibrinogen.

297 ynaptogenic domain and the alpha2delta-1 von-Willebrand-factor domain.

298 -Gamma Induced Protein 10[rs4256246] and von-Willebrand-Factor[rs12829220] in the control group; Chro

299 n-cleaving enzymes (ADAMTS7 and 12), the von-Willebrand Factor proteinase (ADAMTS13) and a group of o

300 for alpha2delta-1 with mutations in the von-Willebrand-factor-A domain.