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VWF was significantly associated with CRP only. Paper-11364059.
Shear tango: dance of the ADAMTS13/ VWF complex. Paper-12918877.
Degradation of FVIII was completely inhibited by vWF. Paper-1964868.
Platelet-derived VWF- cleaving metalloprotease ADAMTS-13. Paper-11533621.
Alternatively, ABO group may affect vWF plasma clearance rates. Paper-10731337.
These conditions would allow VWF to act as a cargo targeting OPG to WPBs. Paper-13409384.
Two recognition sites for vWf binding have been identified on the GPIIb/IIIa. Paper-5535634.
Finally, the effect of the antibodies was tested on vWF binding to GPIIb/IIIa. Paper-2194346.
Effect of ABO blood group on the collagen- binding assay for von Willebrand factor. Paper-9564552.
At E2.5-E3, 90% of cells express only MyHC and 6% express only vWF/Flk-1. Paper-13416959.
After washing, vWf- bound FVIII activity was determined with a chromogenic assay. Paper-43383.
The rise in vWF is associated with that in CRP and with enhanced platelet reactivity. Paper-10692041.
7. Solid-phase vWF (1.2 microg ml(-1)) resulted in the release of MMP-2 from platelets. Paper-9084688.
von Willebrand factor cleaving protease and ADAMTS13 mutations in childhood TTP. Paper-9838221.
Platelet- VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress. Paper-12682861.
Although ABO blood groups influenced VWF levels, they had no influence on ADAMTS13. Paper-13120662.
Surface-immobilized vWF was shown to induce CD62P exposure on the platelet cell surface. Paper-1609780.
ABO blood group influences the clearance rates of VWF rather than VWF secretion rates. Paper-12314617.
Size regulation of von Willebrand factor- mediated platelet thrombi by ADAMTS13 in flowing blood. Paper-10810978.
ADAMTS13 is a metalloproteinase that cleaves von Willebrand factor ( VWF) multimers. Paper-10826395.
In the absence of fibrinogen, however, aggregation was mediated by vWF binding to GPIIb/IIIa. Paper-5536440.
Erk2 is activated in platelets on stimulation with VWF/ristocetin in a time-dependent manner. Paper-10977659.
ADAMTS-13 specifically cleaves a peptidyl bond between Y1605 and M1606 in the A2 domain of VWF. Paper-10204628.
We have used an anti-human vWF MAb W5-6A to investigate the FVIII binding site on vWF. Paper-6494113.
Shear-induced von Willebrand factor- mediated platelet surface translocation of the CD40 ligand. Paper-10688623.
Recently, a metalloprotease that cleaves VWF multimers has been identified, namely ADAMTS13. Paper-13406198.
Similarly, peptide 2013 to 2022 inhibited FVIII binding to VWF by 84% (50% inhibition, 25 microM). Paper-9459708.
Because vWF binding by FVIII involves its light chain, LRP binding to this subunit was studied. Paper-1964868.
Changes in von Willebrand factor- cleaving protease ( ADAMTS13) activity after infusion of desmopressin. Paper-9855751.
beta2-Glycoprotein I inhibits von Willebrand factor dependent platelet adhesion and aggregation. Paper-13400028.
Each vWF subunit contains binding sites for collagen and for platelet glycoproteins GPIb and GPIIb/IIIa. Paper-719313.
VWF release and platelet aggregation in human melanoma after perfusion with TNF alpha. Paper-351658.
Von Willebrand factor targets IL-8 to Weibel-Palade bodies in an endothelial cell line. Paper-9756900.
At high concentrations of ristocetin (1.2 mg/mL), both WT GPIb alpha and M239V specifically bound to 125I- vWF. Paper-1089319.
Efficiency of von Willebrand factor- mediated targeting of interleukin-8 into Weibel-Palade bodies. Paper-12619164.
VEGF and basic fibroblast growth factor can synergistically upregulate the vWF gene expression. Paper-10025929.
The studies demonstrate a shear-dependent role for PI 3-kinase in promoting platelet adhesion on immobilized VWF. Paper-9152561.
TP expression was associated with stromal microvessel density assessed with anti- vWF, but not with anti-CD34. Paper-10061837.
FVIIa induced VWF release from endothelial cells may have in vivo significance at sites of TF expression. Paper-9596667.
A polyclonal antibody made to the Val1670-Glu1684 peptide also demonstrated inhibition of FVIII binding to vWF. Paper-5808085.
Effect of von Willebrand factor Y/C1584 on in vivo protein level and function and interaction with ABO blood group. Paper-13226859.
ABO blood group antigens are covalently associated with asparagine- linked sugar chains of plasma vWF. Paper-8278180.
CONCLUSIONS: The disulfide bonds between GPIbalpha and GPIbbeta are necessary for optimal GPIbalpha binding to VWF. Paper-13025549.
Measurement of plasma von Willebrand factor in acute coronary syndromes and the influence of ABO blood group status. Paper-10867987.
These findings suggest that it is H antigen expression that mediates the ABO effect on plasma vWF concentration. Paper-9372180.
First, below a [Ca2+]i of 500 nmol/L, an increase in Ca2+ was sufficient for vWF release but not for TPA release. Paper-1211242.
p38 MAPK is activated but not necessary in porcine von Willebrand factor-dependent platelet activation. Paper-2074401.
Fifteen monoclonal antibodies against the 52/ 48-kDa fragment inhibited von Willebrand factor binding to collagen. Paper-5175313.
ADAMTS13 is a plasma metalloproteinase that cleaves von Willebrand factor to smaller, less thrombogenic forms. Paper-13263166.
ADAMTS13 in cell lysate or serum-free conditioned medium cleaved von Willebrand factor ( VWF) specifically. Paper-12237484.
Glycoprotein Ibalpha can mediate endothelial cell migration on von Willebrand factor-containing substrata. Paper-8295664.
The proportion of TM-positive microvessels was expressed relative to total von Willebrand factor (vWF)-positive vessels. Paper-9546976.
In this work, we found that VWF stimulated the rapid and sustained phosphorylation of p38 MAP kinase (p38MAPK). Paper-10354047.
Vasopressin-induced vWF secretion is mimicked by DDAVP and inhibited by the selective V2R antagonist SR121463B. Paper-8393968.
Among the numerous variants of vWD, no patient with an abnormal vWF binding to GPIIb/IIIa has been described to date. Paper-2011798.
There was no clear influence of CRP on E-selectin, but 20 and 50 microg/ml CRP inhibited the release of vWF. Paper-9959012.
A significant correlation was observed between von Willebrand factor antigen and activated partial thromboplastin time. Paper-13217242.
METHODS AND RESULTS: In a solid-phase binding assay, VWF was able to bind specifically to OPG in a calcium-dependent manner. Paper-13409384.
Moreover, recombinant PSGL-1 protein and cell surface- expressed PSGL-1 directly interacted with VWF. Paper-12321403.
VWF protects FVIII from endocytosis by dendritic cells and subsequent presentation to immune effectors. Paper-12396686.
A recent study shows that platelets contain the VWF- cleaving metalloprotease ADAMTS-13, but its activity remains unknown. Paper-11533621.
These results revealed that the region between the disintegrin-like and cysteine-rich/spacer domains interacts with VWF. Paper-11396264.
Alpha 2A adrenergic receptor polymorphism is associated with plasma von Willebrand factor levels in a general population. Paper-12876710.
ABO (H) blood group antigens are covalently linked to the oligosaccharide side-chains of von Willebrand factor ( VWF). Paper-8371052.
CD34 was more sensitive and specific than vWf for staining endothelial cells associated with VEGF expression. Paper-8494246.
In HUVEC, OPG co-localizes with P-selectin and von Willebrand factor ( vWF), within the Weibel-Palade bodies (WPB). Paper-10732848.
ADAMTS13 cleaves von Willebrand factor ( VWF) between Tyr(1605) and Met(1606) residues at the central A2 subunit. Paper-13421765.
Monoclonal antibodies directed against GPIb and GPIIb/IIIa as well as EDTA completely inhibited vWF-induced aggregation. Paper-5421792.
Among the genetic factors, only the ABO gene located on chromosome 9q34 has been clearly linked to the plasma levels of vWF. Paper-9915950.
Inhibition of either the NF1 or the R repressor alone is not sufficient to activate the VWF promoter in smooth muscle cells. Paper-1660824.
PAI-1, tPA, tPA/ PAI-1- complex and vWF were measured after two weeks, six and 12 months following randomisation. Paper-9383850.
ABO blood groups appeared to strongly influence VWF clearance, but not its synthesis or release from endothelial cells. Paper-12770784.
This study reinforces the hypothesis of a genetic influence of FVIII levels beyond the influence of VWF:Ag and ABO blood groups. Paper-11269896.
Anti-beta(2) GPI autoantibodies neutralize this inhibitory function and are associated with increased levels of active VWF. Paper-13400028.
The amino-terminus of ADAMTS13 protease appears to be sufficient to bind and cleave VWF under static and denatured condition. Paper-13421765.
The multimeric size of von Willebrand factor ( VWF) is regulated by the specific cleaving metalloprotease, ADAMTS-13. Paper-11491027.
It was concluded that SB203580-inhibitable p38 MAPK activity induced by porcine VWF is not necessary for platelet activation. Paper-2074401.
These data suggest that CTRP-1 prevents collagen- induced platelet aggregation by specific blockade of VWF binding to collagen. Paper-10832898.
Arterial blood flow enhances glycoprotein Ibalpha ( GPIbalpha) binding to vWF, which initiates platelet adhesion to injured vessels. Paper-12927324.
In contrast to human neutrophil elastase, cathepsin G inactivates and degrades vWF not only in BHS but also in cryoprecipitate. Paper-6891095.
Discrepant activity levels of von Willebrand factor- cleaving protease ( ADAMTS-13) in congenital thrombotic thrombocytopenic purpura. Paper-10044104.
Shielding the front-strand beta 3 of the von Willebrand factor A1 domain inhibits its binding to platelet glycoprotein Ibalpha. Paper-9759663.
We conducted this genetic study to test whether the ABO O1 allele is associated with low vWF plasma levels and with a reduced risk of MI. Paper-10457165.
Using a simple enzyme-linked immunosorbent assay, an IgG antibody against vWF is detectable in AvWS associated with SLE and IgG BMG. Paper-12227075.
Patient 1, who is the first cousin of patient 2, had an FVIII binding defect of vWF, low levels of vWF, and multimeric impairment. Paper-8499367.
Deleting the spacer domain from ADAMTS13 or deleting the exosite from the VWF substrate reduced the rate of cleavage approximately 20-fold. Paper-12353753.
Modeling studies revealed that the relative orientation of the alpha helices in VWF TASP led to a clash of bound botrocetin and GPIb alpha. Paper-10442094.
ABO blood groups greatly influence circulating von Willebrand factor ( VWF) levels and O group subjects have lower VWF values. Paper-12770784.
These results indicate that shear-induced VWF binding to platelet GpIb-IX-V stimulates functionally important PI3-K activity. Paper-9877074.
von Willebrand factor release and thrombomodulin and tissue factor expression in Rickettsia conorii-infected endothelial cells. Paper-7530685.
A shorter von Willebrand factor survival in O blood group subjects explains how ABO determinants influence plasma von Willebrand factor. Paper-12770784.
The ABO locus has functional effects on vWF and FVIII levels and is genetically correlated with FVIII, vWF and thrombosis. Paper-11499745.
Recombinant human ADAMTS13 was also less effective in cleaving VWF multimers than VWF73 when the C-terminal TSR sequence was deleted. Paper-13347773.
Mapping of distinct von Willebrand factor domains interacting with platelet GPIb and GPIIb/IIIa and with collagen using monoclonal antibodies. Paper-5409401.
We reproduced these mutations in vWF cDNA and expressed the recombinant proteins in furin cDNA containing baby hamster kidney (fur-BHK) cells. Paper-1944978.
The VWF bead- induced platelet activation was completely inhibited by addition of monoclonal antibody (mAb) to GPIb or GPIIb/IIIa. Paper-1027429.
Present study demonstrates that ADAMTS13 cleaves VWF in a rotation speed- and protease concentration-dependent manner on a mini vortexer. Paper-13421765.
ADAMTS13 and delCUB (but not MDTCS) bind VWF under flow with dissociation constants (K(D)) of about 50 nM and about 274 nM, respectively. Paper-13421765.
ADAMTS-13 rapidly cleaves newly secreted ultralarge von Willebrand factor multimers on the endothelial surface under flowing conditions. Paper-9187541.
The thrombospondin-1 N700S polymorphism is associated with early myocardial infarction without altering von Willebrand factor multimer size. Paper-12080093.
Thus, in addition to alphavbeta3, EC GP Ibalpha initiates ERK activation, and regulates ERK- induced EC migration on vWF. Paper-10711994.
ADAMTS13 controls the multimeric size of circulating von Willebrand factor ( VWF) by cleaving the Tyr1605-Met1606 bond in theA2 domain. Paper-10839557.
Glycoprotein Ib alpha ( GpIb alpha) is a platelet membrane Gp that binds von Willebrand factor and mediates platelet adhesion to subendothelium. Paper-7412193.
Recent advances have shown that TTP is caused by deficiency of a circulating, von Willebrand factor cleaving metalloprotease, ADAMTS13. Paper-13365300.
These results indicate that while the VNR is the primary adhesion receptor for vWF, endothelial GPIb alpha can mediate HUVEC attachment to vWF. Paper-268187.
In conclusion, the alpha 2A adrenergic receptor 2372A/G polymorphism is associated with plasma von Willebrand factor levels in a general population. Paper-12876710.
Based on mutagenesis and kinetic analysis, we find that the ADAMTS13 spacer domain binds to an exosite near the C terminus of the VWF A2 domain. Paper-12353753.
von Willebrand factor- cleaving protease ( ADAMTS13) cleaves von Willebrand factor ( VWF) and regulates its physiologic function. Paper-9855751.
VWF TASP was found to inhibit specifically botrocetin- induced platelet aggregation and to bind both botrocetin and GPIb alpha. Paper-10442094.
The metalloprotease ADAMTS-13 cleaves von Willebrand factor ( VWF) at the Y842/M843 peptide bond located in the A2 domain. Paper-10541414.
Our results indicate that subjects with an abnormal vWF binding to GPIIb/IIIa are probably rare and difficult to target for a specific screening. Paper-2011798.
MA-16N7C2 blocked fibrinogen and von Willebrand factor binding to GPIIb/IIIa in a competitive manner with a Ki of 8.5nM and 13.2nM, respectively. Paper-8148183.
von Willebrand factor binding to platelet glycoprotein Ib-IX-V stimulates the assembly of an alpha-actinin-based signaling complex. Paper-10473112.
In the present study, we demonstrated that VWF- mediated FVIII protection from APC also results from direct inhibition of FVIII binding to APC. Paper-9459708.
This substitution within the vWF- binding region of GP Ib alpha is likely to exert a significant influence on the conformation of the resulting protein. Paper-6881709.
We conclude that, this new method for measurement of plasma or platelet VWF- binding capacity offers great advantages for correct type 2B VWD diagnosis. Paper-12108074.
Thus, below 500 nmol/L [Ca2+]i, an increase in [Ca2+]i alone was sufficient to induce vWF release but not sufficient to induce TPA release. Paper-1211242.
Glycocalicin is the external part of platelet glycoprotein Ib alpha ( GPIb alpha) and contains binding sites for von Willebrand factor and thrombin. Paper-7373846.
Furthermore, vWF binding to GPIb-IX induces phosphorylation of Thr-202/Tyr-204 of extracellular signal-regulated kinase 2 ( ERK2). Paper-9088534.
Antibodies to thrombin-inactivated FVIII/ vWF or normal FVIII/ vWF had about the same ability to inactivate FVIII procoagulant activity. Paper-3325087.
FVIII- LRP interaction involves the FVIII light chain, and FVIII- vWF complex formation plays a regulatory role in LRP binding. Paper-1964868.
The isolated CUB domains are neither sufficient to bind VWF detectably nor capable of inhibiting proteolytic cleavage of VWF by ADAMTS13 under flow. Paper-13421765.
Nonneutralizing IgM and IgG antibodies to von Willebrand factor- cleaving protease ( ADAMTS-13) in a patient with thrombotic thrombocytopenic purpura. Paper-10044129.
When secretion was induced, OPG remained associated with VWF in extracellular patches of release under biochemical conditions found in blood plasma. Paper-13409384.
Furthermore, recombinant ADAMTS13- mediated degradation of VWF multimers was entirely inhibited in the presence of plasma from a patient with acquired TTP. Paper-9331480.
BACKGROUND: The platelet membrane glycoprotein IIb/IIIa functions as a receptor for fibrinogen and von Willebrand factor during platelet aggregation. Paper-1635849.
ADAMTS13 is a plasma metalloproteinase that regulates platelet adhesion and aggregation through cleavage of von Willebrand factor ( VWF) multimers. Paper-11390765.
The finding that an amino acid polymorphism in VWF may influence susceptibility to ADAMTS13 has potentially significant implications in diverse areas. Paper-10204643.
Leucine-rich repeats 2-4 (Leu60-Glu128) of platelet glycoprotein Ibalpha regulate shear-dependent cell adhesion to von Willebrand factor. Paper-12209319.
Recently described viper venom proteins that bind to the GP Ib alpha-chain and inhibit vWF binding provide novel probes for studying receptor function. Paper-696327.
Overexpressed t-PA was detected in Weibel-Palade bodies and acutely released together with endogenous vWf by thrombin or calcium ionophore stimulation. Paper-1918303.
Sequence analysis of the FVIII- binding domain encoded by the vWF mRNA of the affected individual identified mutations in both vWF alleles. Paper-477399.
Levels of plasma Von Willebrand Factor ( vWF) are known to be influenced by ABO Blood Group but such an influence on platelet vWF is not known. Paper-7476062.
Filamin A binding to the cytoplasmic tail of glycoprotein Ibalpha regulates von Willebrand factor-induced platelet activation. Paper-10000356.
The inhibition of wild-type FVIII by LE antibody is enhanced by vWF and is associated with an antibody-dependent reduced rate of FVIIIa release from vWF. Paper-1794914.
On the basis of these results, we hypothesize that an H1-like protein functions as an endothelial cell-specific transcriptional activator of the VWF promoter. Paper-10652631.
By comparison to healthy FVIII, Del2201 FVIII had a significantly reduced binding to VWF, which likely contributes to reduced FVIII levels in plasma. Paper-10214903.
Deficiency of von Willebrand factor ( VWF) cleaving protease ADAMTS13 is associated with the development of thrombotic thrombocytopenic purpura (TTP). Paper-10044102.
ADAMTS13 cleaved VWF and FRETS-VWF73 with roughly comparable catalytic efficiency of 55 microM(-1) min(-1) and 18 microM(-1) min(-1), respectively. Paper-10826395.
The A/T1381 polymorphism in the A1-domain of von Willebrand factor influences the affinity of von Willebrand factor for platelet glycoprotein Ibalpha. Paper-13319016.
The latter finding demonstrates that direct immobilization on a substrate is not a strict requirement for VWF binding to platelet glycoprotein Ibalpha. Paper-9154257.
Above this threshold, active A1 domains become exposed in soluble VWF multimers and can bind to glycoprotein Ibalpha, promoting additional platelet recruitment. Paper-12214117.
Furthermore, we found that IL-8 binds to immobilized VWF under the slightly acidic conditions thought to prevail in the lumen of the late secretory pathway. Paper-12619164.
The activity of von Willebrand factor ( vWF) cleaving metalloprotease ADAMTS13 was low and considered to have contributed to the disease activity of TTP. Paper-12381402.
These results establish that genetic differences in the adhesion receptor subunits alpha(2), alpha(IIb,) and GPVI can influence the phenotype of VWD type 1. Paper-10895055.
von Willebrand factor release and P-selectin expression is stimulated by thrombin and trypsin but not IL-1 in cultured human endothelial cells. Paper-7602466.
It is known that tPA and VWF:Ag are released simply as a result of endothelial stimulation and that the release of TM is preceded by endothelial damage. Paper-7495720.
Interaction of von Willebrand factor with platelets activated by thrombin or a synthetic 7-amino acid peptide derived from the cleaved thrombin receptor. Paper-144683.
Finally, phosphorylation of Pyk2 induced by vWF, but not by thrombin, was inhibited by piceatannol, suggesting that this kinase lies downstream Syk. Paper-9609115.
Results of the collagen-binding assay of ADAMTS13 activity were confirmed in selected samples by testing the capacity of plasma to cleave recombinant VWF A1-A2-A3. Paper-9186525.
Characterization of liposomes carrying von Willebrand factor- binding domain of platelet glycoprotein Ibalpha: a potential substitute for platelet transfusion. Paper-1964759.
Addition of an anti-TNF alpha antibody decreased by 40% E-selectin and ICAM-1 induction and suppressed PAI-1 overproduction with a weak effect on vWf. Paper-1033132.
These data indicate that platelet- vWf released from platelets binds primarily to the GPIIb/IIIa complex at or near the plasma fibrinogen binding site. Paper-5163086.
Solid-phase von Willebrand factor contains a conformationally active RGD motif that mediates endothelial cell adhesion through the alpha v beta 3 receptor. Paper-107418.
Genetic polymorphisms G894T on the eNOS gene is associated with endothelial function and vWF levels in premature myocardial infarction survivors. Paper-10566647.
Src family kinase-mediated and Erk- mediated thromboxane A2 generation are essential for VWF/GPIb-induced fibrinogen receptor activation in human platelets. Paper-10977659.
TM was not significantly different from controls. vWF was significantly increased (P <.01), and its supranormal multimers increased in more than 50% of patients. Paper-9790339.
Independent modulation of von Willebrand factor and fibrinogen binding to the platelet membrane glycoprotein IIb/IIIa complex as demonstrated by monoclonal antibody. Paper-4829703.
The significance of this interaction is unclear, however, because it has not been possible to detect vWf binding to GPIIb/IIIa on platelets stimulated in plasma. Paper-5566356.
Objectives: To determine the mechanisms leading to eNOS activation and clarify the downstream signaling pathways activated by platelet-derived NO in response to VWF. Paper-12314579.
There are data indicating that the regulated acute release of t-PA from the endothelium is closely interrelated with release of von Willebrand factor ( vWF). Paper-1154190.
VWF- mediated increase in platelet thrombi on collagen was not enhanced and indeed was somewhat attenuated by coperfused fibronectin at a shear rate of 5000 s(-1). Paper-12237487.
However, it has been established that the ABO effect is primarily mediated through a direct functional effect of the ABO locus on plasma vWF levels. Paper-10731337.
We conclude that point mutations of the RGDS sequence in vWF selectively impair binding to platelet glycoprotein IIb/IIIa and the HUVEC vitronectin receptor. Paper-52523.
Inhibition of MAP kinase kinase ( MEK) blocks endothelial PGI2 release but has no effect on von Willebrand factor secretion or E-selectin expression. Paper-601094.
Moreover, the use of anti- vWF monoclonal antibodies that inhibit the FVIII binding showed that these 2 mutations likely induce a conformational change in the D' domain. Paper-8499367.
ADAMTS13 could cleave approximately 14% of VWF pretreated with guanidine HCl, suggesting that this substrate is heterogeneous in susceptibility to proteolysis. Paper-10826395.
The proportion of TM-positive microvessels was expressed relative to total vWF-staining vessels, according to vessel caliber and regional distribution within the nerve. Paper-9469879.
Spread GATA-1 platelets bound very few vWF multimers, which were much smaller in size than those on normal spread cells, but were able to move then to cell centers. Paper-13413239.
The ATR/TEM8-PA interaction is mediated by the receptor's extracellular domain related to von Willebrand factor type A or integrin inserted domains (VWA/I domains). Paper-9690056.
In contrast, colocalization of FVIII was not observed when these cells were transfected with plasmids encoding defective FVIII- binding vWf mutants. Paper-1339439.
TF was also positively associated with plasma von Willebrand factor ( vWF) antigen, and inversely associated with activated partial thromboplastin time. Paper-9600593.
GPV-deficient and wild-type platelets were indistinguishable in botrocetin- mediated platelet agglutination and in their ability to adhere to mouse vWF A1 domain. Paper-2054066.
ADAMTS13 is a circulating zinc metalloprotease that cleaves the hemostatic glycoprotein von Willebrand factor ( VWF) in a shear-dependent manner. Paper-11190477.
Peptides, peptidomimetics, and antibodies are generated that competitively block the binding of fibrinogen or von Willebrand factor to the activated GPIIb/IIIa complex. Paper-1427235.
Exons 18-24 of the vWf gene encoding for the first 311 amino acids of mature vWf subunit were amplified by the polymerase chain reaction method and sequenced. Paper-6883248.
ABH antigenic determinants have been identified on the N- linked oligosaccharide chains of circulating vWF and FVIII, according to the blood group of the individual. Paper-10731337.
Von Willebrand factor- cleaving protease ( ADAMTS13) in thrombocytopenic disorders: a severely deficient activity is specific for thrombotic thrombocytopenic purpura. Paper-9186520.
This shear-induced platelet aggregation ( SIPA) is mediated by von Willebrand factor binding to platelet membrane glycoprotein (GP) Ib and GPIIb/IIIa. Paper-168442.
Inhibition of FVIII binding to anhydro-APC by VWF would be consistent with partial or complete overlap of the FVIII binding sites for APC and VWF. Paper-9459708.
von Willebrand factor cleaving protease ( ADAMTS13) is deficient in recurrent and familial thrombotic thrombocytopenic purpura and hemolytic uremic syndrome. Paper-9186525.
In addition, C-reactive protein ( CRP) induced a time- and dose-related release of vWF:Ag from EC, while glucocorticoid did not effect the release of