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 factor (VWF) contains binding sites for plate

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

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

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

11 Von Willebrand factor (VWF) is a key player in the regulatio

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 particularly intriguing cas

15 von Willebrand factor (VWF) is an essential hemostatic prote

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

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

18 Von Willebrand factor (VWF) plays a major role in arterial t

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

20 Von Willebrand factor (VWF), a large multimeric blood protei

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

22 Von Willebrand factor (VWF), an exceptionally large multimer

23 Von Willebrand factor is proposed to be mechanically activat

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

25 Von Willebrand factor, an ultralarge concatemeric blood prot

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

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

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

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

30 R2), endothelial injury (angiopoietin-2, von Willebrand factor, soluble thrombomodulin), impaired oxy

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

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

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

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

35 similar to integrin beta-chains, with a von Willebrand factor A domain containing a functional metal

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

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

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

39 o occur in patients affected by acquired von Willebrand syndrome.

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

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

42 At variance with hemophilia A and B and von Willebrand disease, RCDs are much less prevalent, rangin

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

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

45 idus (DI), bedwetting, haemophilia A and von Willebrand disease.

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

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

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

49 sma osteoprotegerin, angiopoietin-2, and von Willebrand Factor (vWF) levels were measured as biomarke

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

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

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

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

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

55 f established EC markers VE-cadherin and von Willebrand factor (vWF).

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

57 rosine kinase decreased more quickly and von Willebrand factor and thrombomodulin decreased more slow

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

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

60 model with %TBSA, inhalation injury, and von Willebrand factor could be used to better identify at-ri

61 of clotting factor VIII, factor IX, and Von Willebrand Factor knockout (FVIII(-/-), FIX(-/-), and VW

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

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

64 valuated transient elastography (TE) and von Willebrand factor to platelet count ratio (VITRO) as non

65 ibronectin, vitronectin, collagen 1, and von Willebrand factor), strongly suggesting a role for FLNa/

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

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

68 model with %TBSA, inhalation injury, and von Willebrand factor-A2 had comparable discrimination to mo

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

70 ecretion (platelet function markers) and von Willebrand factor.

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

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

73 Forkhead-associated (FHA) and von Willebrand type A (vWA) domains are involved in several

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

75 Caplacizumab, an anti-von Willebrand factor humanized, bivalent variable-domain-on

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

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

78 volving excessive endothelial-associated von Willebrand factor (VWF) and secondary platelet adhesion.

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

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

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

82 e shown an intimate relationship between von Willebrand factor (VWF) multimer profile and heart valve

83 n fragment, inhibits interaction between von Willebrand factor multimers and platelets.

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

85 d the larger, N-terminal, Ca(2+)-binding von Willebrand D domain (VWD) 3 module to form a wedge shape

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

87 macromolecular motions of the biopolymer von Willebrand Factor (vWF) immersed in flow.

88 Intriguingly, blocking von Willebrand factor (VWF) resulted in vascular leaks durin

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

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

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

92 trols, increased levels of calprotectin, von Willebrand factor, angiotensinogen, IL8, IL15, IP10, TNF

93 lling (P-selectin) and platelet capture (von Willebrand factor [VWF]).

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

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

96 al glycosylation has been shown to cause von Willebrand disease (VWD) in a number of different mouse

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

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

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

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

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

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

103 nts microvascular thrombosis by cleaving von Willebrand factor (VWF) within platelet-rich thrombi, an

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

105 PBs) are secretory granules that contain von Willebrand factor and P-selectin, molecules that regulat

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

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

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

109 nors (n = 54) over pooled plasma derived von Willebrand factor (VWF) protein and purified blood type-

110 VN, driven partly by endothelial-derived von Willebrand factor and vascular cell adhesion molecule 1,

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

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

113 Endogenous von Willebrand factor (VWF) stabilizes and protects FVIII fr

114 was associated with reduced endothelial von Willebrand factor expression, which has been shown to me

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

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

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

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

119 otic plaque formation involving enhanced von Willebrand factor exposure on endothelial cells and augm

120 endothelial nitric oxide synthase(eNOS), von Willebrand factor(vWF), and CD31 after cardiac hypertrop

121 n 2, vascular endothelial growth factor, von Willebrand factor, E-selectin, intercellular adhesion mo

122 xpression levels of coagulation factors, von Willebrand factor (vWF), and tissue factor (TF), were de

123 Here we report that, under flow, von Willebrand factor/glycoprotein Ibalpha-dependent platele

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

125 The frequent von Willebrand factor (VWF) variant p.Phe2561Tyr is located

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

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

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

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

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

131 n an independent cohort, we found higher von Willebrand factor levels and equivalent propeptide level

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

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

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

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

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

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

138 independently associated with changes in von Willebrand factor, soluble intercellular adhesion molecu

139 Also, when whole blood was perfused in von Willebrand factor-coated microfluidic channels, platelet

140 eeding tendency), without differences in von Willebrand factor.

141 cell and platelet activation, including von Willebrand Factor (VWF) antigen, soluble thrombomodulin,

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 ocytopathy, counterbalanced by increased von Willebrand factor.

145 ve determined that age, body mass index, von Willebrand factor antigen (VWF:Ag) levels, and ABO blood

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

147 g the catalytic domain together with its von Willebrand domain type A (VWA).

148 actor, soluble fms-like tyrosine kinase, von Willebrand factor, E-selectin, intercellular adhesion mo

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

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

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

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

153 Our structure provides insight into many von Willebrand disease mutations, including those that dimin

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

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

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

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

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

159 res two additional serum factors, namely von Willebrand factor and thrombospondin-1.

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

161 rbed in type 2 dysfunctional subtypes of von Willebrand disease (VWD) by mutations that alter the str

162 responsible for the majority of cases of von Willebrand disease (VWD), the most common inherited huma

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

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

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

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

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

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

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

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

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

172 Moreover, we found that release of von Willebrand factor (VWF) as a result of shear stress is d

173 ticular, ABO affects multiple aspects of von Willebrand factor (VWF) biology.

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

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

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

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

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

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

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

181 This work explores the expression of von Willebrand factor (VWF) on isolated Hc resulting in teth

182 along the surface of extended strings of von Willebrand factor (VWF) released from the endothelium fo

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

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

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

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

187 ADAMTS13 inhibits the growth of von Willebrand factor (VWF)-platelet aggregates by cleaving

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

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

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

191 ss of high-molecular-weight multimers of von Willebrand factor (VWF).

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

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

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

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

196 g-transformed levels of the A2 domain of von Willebrand factor in the first 24 hours was most strongl

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

198 ADAMTS13 allows unrestrained adhesion of von Willebrand factor multimers to platelets and microthromb

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

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

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

202 t triple helix and consists primarily of von Willebrand factor type A (VWA) domains, protein-protein

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

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

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

206 Glycan determinants on von Willebrand factor (VWF) play critical roles in regulatin

207 lly regulate its proteolytic activity on von Willebrand factor (VWF).

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

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

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

211 artial quantitative deficiency of plasma von Willebrand factor (VWF) is responsible for the majority

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

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

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

215 e been previously associated with plasma von Willebrand factor and coagulation factor VIII levels in

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

217 5416 mouse model identified the presence von Willebrand factor/alpha-smooth muscle actin-positive end

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

219 e ER-Golgi trafficking of prohaemostatic von Willebrand factor (VWF) and extracellular matrix (ECM) p

220 s the pro-thrombotic and proinflammatory von Willebrand factor) and presence of neutrophil extracellu

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

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

223 tor VIII (FVIII) and its carrier protein von Willebrand factor (VWF) are associated with risk of arte

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

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

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

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

228 The hemostatic protein von Willebrand factor (VWF) released by endothelial cells (E

229 r the large, multidomain dimeric protein von Willebrand factor (VWF) that is critically involved in p

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

231 mechanosensitive adhesive blood protein, von Willebrand Factor (vWF), interacts with the extracellula

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

233 angiopoietin-2, angiopoietin-2/-1 ratio, von Willebrand factor, and endocan were indicative of compli

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

235 3 clinical trial evaluating recombinant von Willebrand factor (rVWF) for the treatment of hemorrhagi

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

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

238 PRACTICE ADVICE 9: Desmopressin releases von Willebrand factor as its primary hemostatic mechanism.

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

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

241 assessed at admission on plasma samples (von Willebrand factor, angiopoietin-1 and angiopoietin-2, so

242 lls (ECs) synthesize, store, and secrete von Willebrand factor multimeric strings and coagulation fac

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

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

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

246 l (GI) bleeding is distinctive of severe von Willebrand disease (VWD), generally arising in older pat

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

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

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

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

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

252 ed unraveling and elongation of tethered von Willebrand factor (VWF) multimers.

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

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

255 ved for type O patients, suggesting that von Willebrand factor (VWF) half-life, as modified by the AB

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

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

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

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

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

261 The von Willebrand factor (vWF) antigen (vWF-Ag) correlates with

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

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

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

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

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

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

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

269 D assemblies make up half of the von Willebrand factor (VWF), yet are of unknown structure.

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

271 anges from 15 to 19 hours because of the von Willebrand factor chaperone effect.

272 t partners, including alphaIIbbeta3, the von Willebrand factor receptor GPIb-IX-V, the tyrosine kinas

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

274 P), an immune-mediated deficiency of the von Willebrand factor-cleaving protease ADAMTS13 allows unre

275 -free survival; caplacizumab targets the von Willebrand factor-platelet interaction to hasten platele

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

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

278 ivation of unactivated platelets through von Willebrand-factor-mediated processes allowed greater gro

279 ets from type O subjects bound poorly to von Willebrand factor (VWF) of mixed ABOs under arterial she

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

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

282 d vessel damage is highly dependent upon von Willebrand factor (VWF).

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

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

285 ction, fibrin(ogen) deposition, and VWF (von Willebrand factor) expression in brain vessels and VWF c

286 like protein 4), CLDN5 (claudin-5), VWF (von Willebrand factor), and CDH5 (VE-cadherin).

287 D4 in vivo induces the formation of VWF (von Willebrand factor)-platelet strings in mesenteric venule

288 ible factor-1 alpha), survivin, and VWF (Von Willebrand factor).

289 elial growth factor receptor 2], or VWF [von Willebrand Factor]), and tube-like formation.

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

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 carriers of hemophilia A and B, or with von Willebrand disease, have an increased risk of bleeding d

296 ors on the platelet surface binding with von Willebrand factor on the vascular walls.

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.