Click here for the function of VWF.
Edit this page in Wiki Genes - VWF or see Wiki Gene.
Shear tango: dance of the ADAMTS13/ VWF complex. Paper-12918877.
Degradation of FVIII was completely inhibited by vWF. Paper-1964868.
Alternatively, ABO group may affect vWF plasma clearance rates. Paper-10731337.
Treatment of ECs with exogenous vWF also stimulated hMSC adhesion. Paper-13590688.
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.
Effect of ABO blood group on the collagen- binding assay for von Willebrand factor. Paper-9564552.
Finally, the effect of the antibodies was tested on vWF binding to GPIIb/IIIa. Paper-2194346.
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.
Fg caused a dose-dependent increase in ET-1 formation and release of vWF from the RHMECs. Paper-13694193.
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.
In the absence of fibrinogen, however, aggregation was mediated by vWF binding to GPIIb/IIIa. Paper-5536440.
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.
Platelet- VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress. Paper-12682861.
Because vWF binding by FVIII involves its light chain, LRP binding to this subunit was studied. Paper-1964868.
These data support the evidence that the GPIIb/IIIa has two distinct binding sites for vWf binding. Paper-5535634.
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.
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.
Erk2 is activated in platelets on stimulation with VWF/ ristocetin in a time-dependent manner. Paper-10977659.
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 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.
Phospholipase D1 is specifically required for regulated secretion of von Willebrand factor from endothelial cells. Paper-13585621.
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.
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.
Anti-beta(2) GPI autoantibodies neutralize this inhibitory function and are associated with increased levels of active VWF. Paper-13400028.
Among the genetic factors, only the ABO gene located on chromosome 9q34 has been clearly linked to the plasma levels of vWF. Paper-9915950.
Monoclonal antibodies directed against GPIb and GPIIb/IIIa as well as EDTA completely inhibited vWF-induced aggregation. Paper-5421792.
Inhibition of either the NF1 or the R repressor alone is not sufficient to activate the VWF promoter in smooth muscle cells. Paper-1660824.
LPS- mediated repression of the VWF promoter was unaffected by the GATA mutation. Paper-13929430.
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.
It was concluded that SB203580-inhibitable p38 MAPK activity induced by porcine VWF is not necessary for platelet activation. Paper-2074401.
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.
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.
Shielding the front-strand beta 3 of the von Willebrand factor A1 domain inhibits its binding to platelet glycoprotein Ibalpha. Paper-9759663.
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.
Mutations impairing FVIII stability in plasma, by reducing FVIII binding to von Willebrand factor ( VWF) were also characterized. Paper-9932161.
The ABO locus has functional effects on vWF and FVIII levels and is genetically correlated with FVIII, vWF and thrombosis. Paper-11499745.
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.
CONCLUSIONS: Our findings demonstrate that FVIII trafficking to WPBs is independent of Tyr1680 and high-affinity binding to VWF. Paper-12532545.
The VWF bead- induced platelet activation was completely inhibited by addition of monoclonal antibody (mAb) to GPIb or GPIIb/IIIa. Paper-1027429.
ADAMTS13 cleaves von Willebrand factor ( VWF) between Tyr(1605) and Met(1606) residues at the central A2 subunit. 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.
These results indicate that the RGDS binds with higher affinity to a vWf binding site on GPIIb/IIIa than does the pentadecapeptide site. Paper-5535634.
Thus, in addition to alphavbeta3, EC GP Ibalpha initiates ERK activation, and regulates ERK- induced EC migration on vWF. Paper-10711994.
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 HUVEC, OPG co-localizes with P-selectin and von Willebrand factor ( vWF), within the Weibel-Palade bodies (WPB). Paper-10732848.
In conclusion, the alpha 2A adrenergic receptor 2372A/G polymorphism is associated with plasma von Willebrand factor levels in a general population. Paper-12876710.
The amino-terminus of ADAMTS13 protease appears to be sufficient to bind and cleave VWF under static and denatured condition. Paper-13421765.
von Willebrand factor- cleaving protease ( ADAMTS13) cleaves von Willebrand factor ( VWF) and regulates its physiologic function. Paper-9855751.
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.
The metalloprotease ADAMTS-13 cleaves von Willebrand factor ( VWF) at the Y842/M843 peptide bond located in the A2 domain. Paper-10541414.
VWF TASP was found to inhibit specifically botrocetin- induced platelet aggregation and to bind both botrocetin and GPIb alpha. Paper-10442094.
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.
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.
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.
Nonneutralizing IgM and IgG antibodies to von Willebrand factor- cleaving protease ( ADAMTS-13) in a patient with thrombotic thrombocytopenic purpura. Paper-10044129.
FVIII- LRP interaction involves the FVIII light chain, and FVIII- vWF complex formation plays a regulatory role in LRP binding. Paper-1964868.
The amount of ET-1 formed and the concentration of released von Willebrand factor ( vWF) in the cell culture medium were measured by ELISAs. Paper-13694193.
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.
Recombinant human ADAMTS13 was also less effective in cleaving VWF multimers than VWF73 when the C-terminal TSR sequence was deleted. Paper-13347773.
This is the first report of a gain-of-function mutation in the GPIbalpha receptor outside the VWF- binding domain in patients with PT- VWD. Paper-11103535.
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.
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.
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.
Above this threshold, active A1 domains become exposed in soluble VWF multimers and can bind to glycoprotein Ibalpha, promoting additional platelet recruitment. Paper-12214117.
The latter finding demonstrates that direct immobilization on a substrate is not a strict requirement for VWF binding to platelet glycoprotein Ibalpha. Paper-9154257.
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.
The data indicate that vWF supports CRC54- induced platelet aggregation via interaction with two receptors--GP IIb-IIIa and GP Ib. Paper-11521155.
These results are consistent with the hypothesis that activation of apoptotic signaling pathways in ECs releases vWF which regulates hMSC adhesion to ECs. Paper-13590688.
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.
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.
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.
Recent studies have demonstrated that deficiency in the von Willebrand factor cleaving protease ADAMTS13, due to genetic mutations or autoimmune inhibitors, causes TTP. Paper-9816944.
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.
Von Willebrand factor- cleaving protease ( ADAMTS13) in thrombocytopenic disorders: a severely deficient activity is specific for thrombotic thrombocytopenic purpura. Paper-9186520.
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.
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 vWF:Ag from EC. Paper-7581935.
Structural analysis of recombinant von Willebrand factor produced at industrial scale fermentation of transformed CHO cells co-expressing recombinant furin. Paper-429771.
Here, we demonstrate that VWF protects FVIII from being endocytosed by human dendritic cells (DCs) and subsequently presented to FVIII-specific T cells. Paper-12396686.
This study indicates that functional expression of the vWF- binding domain of GpIb alpha on the surface of mammalian cells can be obtained in the absence of GpIb beta and GpIX. Paper-917080.
A transient correction of both FVIII:C and vWF parameters to normal for a few weeks after high-dose intravenous immunoglobulin is seen in AvWS associated with SLE and IgG BMG. Paper-12227075.
Activation of pp125FAK by type 2B recombinant von Willebrand factor binding to platelet GPIb at a high shear rate occurs independently of alpha IIb beta 3 engagement. Paper-9728006.
The FVIII- binding defect of vWF containing either mutation alone is approximately half that of the double mutant, which suggests that the effect of these mutations is additive. Paper-477399.
An IAP retrotransposon in the mouse ADAMTS13 gene creates ADAMTS13 variant proteins that are less effective in cleaving von Willebrand factor multimers. Paper-13347773.
Cytochalasin D ( CD) and monobromobimane (MB) enhanced agglutination and prevented the inhibitory action of ADP on bovine vWf-induced platelet agglutination. Paper-19106.
Von Willebrand factor cleaving protease ( ADAMTS-13) in 123 patients with connective tissue diseases ( systemic lupus erythematosus and systemic sclerosis). Paper-9952054.
The sulfation of the 3 tyrosine residues 276, 278, and 279 in GPIb alpha is an important posttranslational modification that seems to promote the interaction with VWF. Paper-9472185.
GpIb alpha contains binding sites for von Willebrand factor and for thrombin and mediates platelet adhesion to the subendothelium under conditions of high shear stress. Paper-1196815.
Analogous to VWF-platelet interaction, VWF provided binding sites for leukocyte receptors involved in rolling ( PSGL-1) and stable (beta2-integrins) adhesion. Paper-12321403.
In this report, we describe the case of a vWD patient who has an abnormal vWF multimers distribution associated with a markedly decreased vWF ability to bind FVIII. Paper-1707918.
Incubation of FVIII/ vWF with proteolytic enzymes causes rapid inactivation of the FVIII procoagulant activity but has little effect on the vWF activity or antigenicity. Paper-3325087.
CONCLUSIONS: These results demonstrate that TPA inhibits platelet aggregation in response to pathological shear stress by altering the multimeric composition of vWf. Paper-345159.
Severely deficient activity of the von Willebrand Factor ( VWF) cleaving metalloprotease, ADAMTS13, is associated with thrombotic thrombocytopenic purpura (TTP). Paper-12134365.
Shear stress triggers von Willebrand factor ( VWF) binding to platelet glycoprotein Ibalpha and subsequent integrin alpha(IIb)beta(3)-dependent platelet aggregation. Paper-10309910.
Experiments using platelets from a patient completely lacking von Willebrand factor showed that von Willebrand factor is not involved in platelet binding to thrombospondin-1. Paper-9769298.
Genetic polymorphisms G894T on the eNOS gene is associated with endothelial function and vWF levels in premature myocardial infarction survivors. Paper-10566647.
Osteoprotegerin ( OPG) is localized to the Weibel-Palade bodies of human vascular endothelial cells and is physically associated with von Willebrand factor. Paper-10732848.
ATP augments von Willebrand factor-dependent shear- induced platelet aggregation through Ca2+-calmodulin and myosin light chain kinase activation. Paper-10309910.
This mutation prevents FVIII binding to a human monoclonal antibody recognizing the C2 domain and inhibiting FVIII binding to VWF and phospholipids. Paper-10214903.
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.
A high exposure of CD62P on the platelet surface was seen after 10 min of incubation on platelets interacting with vWF and normal plasma-coated surfaces (79 and 67%, respectively). Paper-10720865.
In the search for potential antithrombotic properties of beta(2) GPI, we found that beta(2) GPI inhibits von Willebrand factor (VWF)-induced platelet aggregation. Paper-13400028.
Several mutations spread across the ADAMTS13 gene have been identified in association with a deficiency of VWF- cleaving proteinase activity in patients with congenital TTP. Paper-10204629.
In contrast, GPIIb/IIIa similarly bound to the other vWF, independently of the proteic environment, the factor VIII level, the degree of multimerization or the mutation of vWF. Paper-2011798.
Both factors are secreted after intraendothelial Ca2+ mobilization, but exhibit opposing physiological effects with vWF inducing coagulation and tPA triggering fibrinolysis. Paper-10486596.
Platelet attachment is mediated through the interaction of the glycoprotein ( Gp) Ibalpha subunit of the platelet GpIb-IX-V complex with the A1 domain of VWF. Paper-10777659.
In the immunocytochemical study, cytokeratin ( epithelial cell marker) was expressed in all cultured cells. but von Willebrand factor ( endothelial cell marker) was not. Paper-8736051.
These findings confirm that a normal consensus sequence for VWF propeptide cleavage and efficient cleavage are required in vivo for normal FVIII binding capacity of VWF. Paper-9787327.
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.
Purified A2 domain of von Willebrand factor binds to the active conformation of von Willebrand factor and blocks the interaction with platelet glycoprotein Ibalpha. Paper-13351599.
Thus, PKA-mediated phosphorylation of GPIbbeta at Ser(166) negatively regulates VWF binding to GPIb-IX and is one of the mechanisms by which PKA mediates platelet inhibition. Paper-9292865.
Immunofluorescence microscopy of EC infected with GH-containing recombinant adenovirus (GHrAd) demonstrated a granular distribution of GH that colocalized with vWF. Paper-8278175.
Type 2-like AvWS in children with congenital heart valve defects is caused by shear stress- induced proteolysis of large vWF multimers and is reversible after surgical correction. Paper-12227075.
In healthy 20- to 50-year-old women, the ABO blood group has a significant effect on levels of von Willebrand factor (VWF:Ag, formerly VIIIR:Ag) and on factor VIII activity (F.VIII:C). Paper-6120257.
Normal platelets incubated with monoclonal antibodies directed against the fibrinogen and vWf binding site(s) on the GPIIb/IIIa were not aggregated by the type IIb platelet lysate. Paper-6484604.
Von Willebrand factor ( VWF) is secreted as ultralarge multimers that are cleaved in the A2 domain by the metalloprotease ADAMTS13 to give smaller multimers. Paper-13823491.
In conclusion, carriership of Asp299 and Thr399Ile TLR-4 gene polymorphisms is associated with lower levels of sP-selectin and von Willebrand factor among hypercholesterolemic patients. Paper-12483103.
The ScFv gene of phage clone 28 that has best binding activity to VWF-A1 was cloned into pET20b vector for higher expression in E. coli strain BL-21(DE3) pLysS. Paper-11248836.
In marked contrast, in the presence of ristocetin, VWF stimulates formation of fully spread lamellipodia through a pathway that is dependent upon alpha(IIb)beta3 and PI3-kinase. Paper-12108946.
Comparison of von Willebrand factor antigen, von Willebrand factor- cleaving protease and protein S in blood components used for treatment of thrombotic thrombocytopenic purpura. Paper-10550668.
W5-6A inhibited FVIII binding to vWF-coated polystyrene tubes in a concentration-dependent manner with 90% inhibition of FVIII binding at a concentration of 10 micrograms/ml. Paper-6494113.
Using three-color FCM, marrow MKs labeled for GPIIb/IIIa and stained for DNA expressed high levels of von Willebrand factor with a high resolution of 2N/4N MKs from the total marrow cells. Paper-11676948.
To investigate whether ABO influences the rate of VWF synthesis, we performed stable transfection of A transferase in a phenotypically group-O endothelial cell line (EAhy926). Paper-9817639.
TSP1- VWF interactions do not strictly enhance platelet recruitment and secreted TSP1 even weakly competes with the dynamic platelet rolling and adhesion onto VWF. Paper-13034704.
The first stage in hemostasis is the binding of the platelet membrane receptor glycoprotein ( GP) Ib-IX complex to the A1 domain of von Willebrand factor in the subendothelium. Paper-10784095.
In adults, after in vitro activation of platelets with thrombin and ADP, VWF binding to platelets increased and correlated significantly with CD62P expression (r = 0.71, p < 0.001). Paper-10180855.
We also demonstrated that GATA6 is the GATA family member that interacts with the VWF promoter and that GATA6 is associated with NFY specifically in non-endothelial cells. Paper-9858683.
Amount of H antigen expressed on circulating von Willebrand factor is modified by ABO blood group genotype and is a major determinant of plasma von Willebrand factor antigen levels. Paper-9372180.
In the tumor periphery, Ang2 was highly expressed and many small vessels stained positively for von Willebrand factor but not for alpha smooth muscle actin, suggesting angiogenesis. Paper-9045787.
The localization of filamentous actin and the Arp2/3 complex in platelets on VWF in the presence of botrocetin and ristocetin are distinct, yielding disparate lamellipodium kinetic signatures. Paper-12108946.
In previous reports, plasmin was shown in vitro to inactivate FVIII and cleave the vWF subunit extensively, but to cause only a modest decrease in vWF platelet-agglutinating activity. Paper-5126609.
Additionally, preincubation of HUVEC with a synthetic peptide Arg-Gly-Asp (RGD) that prevents vWf- mediated adhesion of SS RBC reduced the surface expression of VCAM-1 and NF-kB activation. Paper-1654827.
Conclusions: We demonstrate that VWF activates eNOS through a specific Ca(2+)-dependent GPIb receptor-signaling cascade that relies on the generation of platelet-derived ADP and TxA(2). Paper-12314579.
The dissociation constant (Kd) for 125I- vWF binding to the recombinant 110-kDa protein was 1.2 +/- 0.2 nM as compared with 1.0 +/- 0.3 nM for vWF binding to purified platelet GP Ib-IX. Paper-100135.
The activation of the von Willebrand factor (vWF)--glycoprotein Ib pathway with botrocetin together with vWF failed to induce Pyk2 (and FAK) tyrosine phosphorylation. Paper-8571607.
These studies demonstrate that platelet aggregation is triggered by the initial interaction of IIB vWF with GPIb which is followed by exposure of fibrinogen binding sites on GPIIb/IIIa. Paper-5130426.
The VWF- cleaving proteinase activity of the truncated enzyme was comparable to that of the wild-type enzyme but its secretion from transfected COS-7 cells was about 14% of the wild type. Paper-10204629.
The change in serum OPG levels during L-T4 replacement therapy was significantly and independently associated in a negative fashion with baseline vWF (r = -0.503, P = 0.0014). Paper-10767437.
Complete inhibition of endothelial cell adhesion to vWF was obtained in the presence of F(ab')2 of monoclonal antibody 9 to vWF, which blocks vWF binding to platelet GPIIb/IIIa. Paper-107418.
This study shows that asialo, and possibly native, vWF acts as a platelet agonist after its binding to GPIb and induces aggregation through a pathway dependent on GPIIb/IIIa-related receptors. Paper-4827226.
These findings indicate that the spontaneous platelet aggregation in this patient results from the binding of her vWF to GPIb but is independent from the binding of her vWF to GPIIb/IIIa. Paper-14955.
We hypothesized that an inhibitor of the GPIb a - von Willebrand factor ( vWF) interaction would be more effective in suppressing MP formation and thrombin generation than GPIIb/IIIa inhibitors. Paper-12341432.
However, vWF(R53W) exhibited the same defect in FVIII binding as did plasma vWF from patients with vWD Normandy, confirming that this mutation is responsible for the vWD Normandy phenotype. Paper-7256851.
The results suggest that vWF domain A1 inhibits the cleavage of domain A2, and that inhibition can be relieved by interaction of domain A1 with platelet GPIbalpha or certain glycosaminoglycans. Paper-10362594.
RESULTS: The A2 domain polypeptide bound specifically to the immobilized A1 domain polypeptide or full-length VWF, with half-maximal binding being obtained at 60 or 168 nm, respectively. Paper-13351599.
The enhanced reactivity of FVIII/ vWF in Type IIB was evident in studies of ristocetin- induced platelet agglutination and of binding of FVIII/ vWF to platelets in the presence of ristocetin. Paper-3631253.
By immunofluorescence microscopy, granular colocalization of GH with endogenous tissue-type plasminogen activator ( tPA) was also demonstrated, and most of the tPA colocalized with vWF. Paper-8278175.
Gain of von Willebrand factor- binding function by mutagenesis of a species-conserved residue within the leucine-rich repeat region of platelet glycoprotein Ibalpha. Paper-11068117.
In the overall population, the changes in vWF antigen and vWF-collagen- binding induced by angioplasty correlated with those in CRP levels (r = 0.47, P = 0.004 and r = 0.44, P = 0.008). Paper-10692041.
We investigated the role in VWF binding of charged residues in the LRR region of GP Ibalpha that are conserved in human, canine, and murine proteins. Paper-11068117.
Immunofluorescent stainings showed EGFP expression exclusively in vascular-like structures simultaneously expressing von Willebrand factor and in formerly beating areas expressing alpha-actinin. Paper-12874230.
Reanalysis of plasma VWF cleaving protease activity using a different assay revealed that the patient had less than 0.1 U/L ADAMTS13 protease activity, while the parents were both partially deficient. Paper-10044102.
Studies with added von Willebrand factor ( vWf) indicate that in the context of thrombin activation vWf activates platelets through mechanisms independent of GPIIb/IIIa to promote PT activity. Paper-1592802.
We also determined serum tumor necrosis factor-alpha ( TNF-alpha), the phenotypes of the IL-8 binding Duffy blood group antigen receptor and the von Willebrand factor ( vWF) plasma levels. Paper-9600581.
We have now grafted a portion of the extracellular domain of GpIb alpha containing the vWF binding site onto the transmembrane/intracellular domain of the single chain surface molecule ICAM-1. Paper-917080.
The latter requires binding of the platelet receptor GPIbalpha to the A1- binding domain of von Willebrand factor ( VWF), which first has to be immobilized from the flowing blood onto the site of injury. Paper-13579151.
The purified FVIII/ VWF complex at 6.0 and 12 microg/ml agglutinates rabbit and bovine erythrocytes, and showed negative agglutination with erythrocytes from other species including human ABO. Paper-13663278.
ABO blood group also influences the von Willebrand factor ( VWF) antigen level in heterozygous carriers of VWF null alleles, type 2N mutation Arg854GIn, and the missense mutation Cys2362Phe. Paper-9542981.
In contrast, a monoclonal antibody that blocks the receptor for adhesive proteins on the platelet GPIIb/IIIa complex failed to inhibit the initial response of platelets to high concentrations of IIB vWF. Paper-5536440.
Calpain proteolysis of von Willebrand factor enhances its binding to platelet membrane glycoprotein IIb/IIIa: an explanation for platelet aggregation in thrombotic thrombocytopenic purpura. Paper-6676757.
The newer ELISA techniques based on VWF binding with factor VIII glycoprotein ( Gp) 1b and cerebrosides have also helped in determining certain unusual forms of VWD. Paper-11586143.
In endothelial cells treated with secretagogues that stimulate vWf release the elongated structures positive for PADGEM disappeared, further identifying these structures as Weibel-Palade bodies. Paper-6491965.
The C2 domain of factor VIII ( FVIII) mediates FVIII binding to von Willebrand factor ( VWF) and phospholipids (PLs), thereby determining the stability and the activity of FVIII. Paper-10214903.
Although its endothelial storage compartment is still not well defined, t-PA release is often accompanied by release of von Willebrand factor ( vWf), a protein stored in Weibel-Palade bodies. Paper-1918303.
We also provide evidence during rolling and adhesion of platelets to vWF that platelet GPIb- vWF interaction triggers alphaIIbbeta3 activation in a JNK1-dependent manner. Paper-12534150.
Neither the blockade of the membrane FCgammaRIIA by a specific monoclonal antibody or the prevention of thromboxane A(2) synthesis by cyclooxygenase inhibitors affected VWF-induced p38MAPK activation. Paper-10354047.
Isolated intact human neutrophils cleave FRETS-VWF73 at the V(1607)-T(1608) peptide bond, suggesting that elastase or PR3 expressed on leukocyte surfaces might cleave VWF. Paper-13943275.
We conclude that the inverse correlation between ADAMTS13 and VWF-related parameters suggests a consumption of ADAMTS13 after the desmopressin- induced release of higher multimers of VWF. Paper-9855751.
Thus, binding of vWF to its major physiological ligands may promote the feedback inhibition of platelet adhesion by stimulating the cleavage of domain A2 by ADAMTS13 independent of fluid shear stress. Paper-10362594.
Patho/physiological platelet aggregate ( thrombus) formation is initiated by engagement of platelet surface receptors, glycoprotein (GP)Ib-IX-V and GPVI that bind von Willebrand factor or collagen. Paper-10447710.
Adhesion receptor activation of phosphatidylinositol 3-kinase. von Willebrand factor stimulates the cytoskeletal association and activation of phosphatidylinositol 3-kinase and pp60c-src in human platelets. Paper-136378.
These data indicate that 2 regions within the sequence Arg218 to Tyr228 have important roles in VWF binding: the alpha1 helix has a regulatory role and the beta turn and beta13 strand bind VWF directly. Paper-10562236.
CONCLUSIONS: The presence of 894T allele on eNOS gene is associated with impaired endothelial function and higher levels of von Willebrand factor in relatively young patients with myocardial infarction. Paper-10566647.
OPG is physically associated with von Willebrand factor ( VWF), a glycoprotein involved in primary hemostasis, within the Weibel-Palade bodies (WPBs) of endothelial cells and in plasma. Paper-13409384.
The anti-C2 monoclonal antibody ESH8, which recognizes residues 2248-2285 and does not inhibit FVIII binding to von Willebrand factor or phospholipid, inhibited FVIII activation by FXa in a clotting assay. Paper-8299697.
CONCLUSIONS: These observations indicate that the sorting efficiency of IL-8 into the regulated secretory pathway of the endothelium is tightly controlled by the entry of VWF into WPBs. Paper-12619164.
Src family kinase-mediated and Erk- mediated thromboxane A2 generation are essential for VWF/GPIb-induced fibrinogen receptor activation in human platelets. Paper-10977659.
Moreover, shear-induced vWF binding was blocked equally effectively by selected monoclonal antibodies against either GP Ib alpha or GP IIb-IIIa or against the respective binding sites in vWF. Paper-377080.
CLB-RAg 35 also inhibited the ristocetin-induced platelet aggregation and the binding of FVIII- VWF to the platelet in the presence of ristocetin but did not affect the binding of FVIII- VWF to collagen. Paper-4819406.
However, the antibody directed against GPIIb/IIIa inhibited 72% of the thrombin- induced increase in the platelet- vWf bound to the platelet surface when platelets were stimulated in the presence of 5 mmol/L Ca++. Paper-5163086.
BACKGROUND: The zinc metalloprotease ADAMTS13 is a multidomain protein that cleaves von Willebrand Factor ( VWF) and is implicated in Thrombotic Thrombocytopenic Purpura (TTP) pathogenesis. Paper-13916117.
This led to the identification of a linear GP Ib alpha sequence (residues Ser251-Tyr279) that effectively inhibited platelet interaction with vWF mediated by ristocetin and, at higher concentration, also by botrocetin. Paper-1794.
Purified normal human fibrinogen inhibited the surface binding of platelet- vWf to thrombin- stimulated platelets to a degree similar to that observed with the monoclonal antibody directed against the GPIIb/IIIa complex. Paper-5163086.
The O blood type and alpha 2A adrenergic receptor 2372AA genotype were significantly associated with lower von Willebrand factor levels, though von Willebrand factor -1051G/A polymorphism did not affect them. Paper-12876710.
Measurement of von Willebrand factor binding to a recombinant fragment of glycoprotein Ibalpha in an enzyme-linked immunosorbent assay-based method: performances in patients with type 2B von Willebrand disease. Paper-12108074.
Glycoprotein ( GP) Ib-IX-transfected cells roll on a von Willebrand factor matrix under flow. Importance of the GPib/actin- binding protein ( ABP-280) interaction in maintaining adhesion under high shear. Paper-1772093.
The protective effect of von Willebrand factor ( VWF) toward activated protein C (APC)- catalyzed inactivation of factor VIII ( FVIII) has been attributed mainly to inhibition of FVIII binding to phospholipid. Paper-9459708.
Since platelets are regarded as a tissue compartment of vWF our findings seem to suggest that the presence of vWF and its release from endothelial cells is required for a normal concomitant release of t-PA. Paper-7258586.
However, aggregation stimulated in the presence of vWF was also completely inhibited by monoAB AK2 directed against GP Ib and capable of blocking its binding with vWF. Paper-11521155.
The interaction between FVIII and CD206 was blocked by VWF, suggesting that, under physiological conditions, the intrinsic mannose-dependent immunogenicity of FVIII is quenched by endogenous immunochaperones. Paper-13253361.
Interaction with glycoprotein Ibalpha was assessed by testing inhibition of monoclonal antibody LJ-Ib1 binding to platelets and inhibition of shear- induced platelet aggregation mediated by native vWF. Paper-538559.
The results of the present study demonstrate that independent modulation of vWF and fibrinogen binding to stimulated platelets can be attained with monoclonal antibodies directed against distinct epitopes of GPIIb/IIIa. Paper-4829703.
CONCLUSIONS: The recombinant A2 domain polypeptide specifically binds to the active conformation of the A1 domain in VWF and effectively blocks the interaction with platelet GPIbalpha under high-flow conditions. Paper-13351599.
BACKGROUND: Thrombotic microangiopathy may develop after solid organ transplantation, but it is usually not associated with severe deficiency in von Willebrand factor- cleaving metalloprotease ( ADAMTS 13) activity. Paper-12046650.
VWF- cleaving protease activity (VWF:CP) and protein S ( PS) levels (total and free antigen and activity) were within the conventional FFP reference range for test and control CSP. Paper-11095173.
Analysis of the binding of FVIII by full-length vWF transiently expressed in COS-7 cells confirms that the combined R19W and H54Q substitutions are the cause of the defective vWF/ FVIII interaction in this patient. Paper-477399.
Addition of the TSP1 5-8 (T5-8CUB) or TSP1 2-8 repeats (T2-8CUB) to the CUB domains restores the binding affinity toward VWF and the inhibitory effect on cleavage of VWF by ADAMTS13 under flow. Paper-13421765.
The dissociation constants of ristocetin-induced (125)I-labelled VWF binding to two forms of soluble recombinant GPIb alpha [(1)His-(302)Ala, either (145)Thr (145T) or (145)Met (145M)] were not different. Paper-10779993.
The patient's hemostatic phenotype was characterized by a mild decrease in plasma factor VIII ( FVIII) and VWF, a decrease in plasma VWF multimers, and a mild reduction in the FVIII binding capacity of VWF. Paper-9787327.
These results illustrate the importance of Arg 53 of the mature vWF subunit for the binding of FVIII to vWF, and identify an amino acid residue within a disulfide loop not previously known to be involved in this interaction. Paper-7256851.
The metalloproteinase ADAMTS13 regulates the size of released von Willebrand factor ( VWF) multimers bound to endothelial cells, but it is unknown whether it can cleave plasma VWF during thrombogenesis. Paper-10810978.
The binding of CD36 to rHuADAMTS13 with retention of its enzymatic activity is consistent with a proposed role for CD36 in localizing ADAMTS13 on the endothelial cell surface where it regulates the cleavage of VWF. Paper-13733892.
Reciprocal immunoprecipitation experiments revealed that while not associated with P-Selectin, OPG is physically complexed with vWF both within the WPB and following secretion from endothelial cells. Paper-10732848.
Of the many GP Ibalpha monoclonal antibodies described, AP1 is of particular interest because it blocks static VWF binding induced by 2 modulators, ristocetin and botrocetin, and platelet adhesion to VWF surfaces under flow. Paper-10562236.
Severe deficiency of the von Willebrand factor (VWF)- cleaving protease ADAMTS13 can lead to thrombotic thrombocytopenic purpura (TTP), a disease associated with the widespread formation of platelet-rich thrombi in many organs. Paper-10319690.
Thus, specific interaction of cysteine-rich domain-containing SVMPs with VWF may function to promote the hemorrhage caused by SVMP proteolysis of capillary basements and surrounding stromal extracellular matrix. Paper-13336200.
We conclude that reduction in the number of terminal sugars on N-linked glycan increases susceptibility of globular VWF to ADAMTS13 proteolysis and is associated with reduced plasma VWF:Ag and VWF:CB levels. Paper-10753090.
BACKGROUND: von Willebrand factor ( VWF) plays a critical role in the process of hemostasis by mediating flow-dependent adhesion and spreading of platelets on exposed extracellular matrix proteins following vascular injury. Paper-12108946.
BACKGROUND: Thrombotic thrombocytopenic purpura (TTP) is associated with congenital and acquired deficiency of ADAMTS-13, a metalloprotease that cleaves von Willebrand factor ( VWF) and reduces its adhesive activity. Paper-12219562.
We describe here the mechanism of platelet adhesion to immobilized von Willebrand factor ( VWF) and subsequent formation of platelet-derived microparticles mediated by glycoprotein Ibalpha ( GPIbalpha) under high shear stress. Paper-11843157.
Objectives of this study were to determine if ACE and MTHFR gene polymorphisms are associated with von Willebrand factor ( vWF) activity, an endothelial dysfunction marker, and with a distinct headache phenotype. Paper-13939106.
Fourth, CVX binding to GPIb alpha is disrupted by phenylalanine substitutions at GPIb alpha tyrosine-276, tyrosine-278, and tyrosine-279, which also disrupts von Willebrand factor and alpha-thrombin binding to GPIb alpha. Paper-10144240.
We have characterised an oligonucleotide G-quartet ( T30923) that specifically blocks VWF binding to GP Ibalpha, the VWF- binding subunit of the GP Ib-IX-V complex. Paper-13962727.
CONCLUSIONS: Our study demonstrated in vitro protective effect of ATA on the inhibition of endothelial activation and vWF secretion and confirmed detrimental effect of ATA on induction of endothelial TF and platelet activation. Paper-13059937.
Deletion of alanine 2201 in the FVIII C2 domain results in mild hemophilia A by impairing FVIII binding to VWF and phospholipids and destroys a major FVIII antigenic determinant involved in inhibitor development. Paper-10214903.
These results indicate that endothelial cell adhesion to vWF is mediated by an RGD-dependent interaction with alpha v beta 3, but does not seem to involve a GPIb-like receptor, and show the importance of the conformation of the RGD sequence. Paper-107418.
It has now been 3 years since the von Willebrand factor (VWF)- cleaving protease implicated in thrombocytopenic purpura (TTP) pathogenesis was identified as ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type 1 motif 13). Paper-10752260.
The formation of these small aggregates was inhibited by monoclonal antibody against GPIIb/IIIa blocking fibrinogen binding to GPIIb/IIIa but not inhibited at all by monoclonal antibody against GPIb blocking vWF binding to GPIb. Paper-8282006.
The platelet glycoprotein ( GP) Ib-IX-V receptor complex has a central role in primary haemostasis and possesses binding sites for the plasmatic adhesive protein von Willebrand Factor ( VWF) and thrombin. Paper-10984141.
CONCLUSIONS: These results suggest that pathological shear-induced VWF binding to GpIb-IX-V stimulates PIP3 production through the assembly of an alpha-actinin-based complex that colocalizes PI 3- KIA with substrate PIP2. Paper-10473112.
Coexpression of wild-type and Arg760Cys VWF into a Furin- producing BHK cell line resulted in decreased VWF secretion and a defect in the FVIII binding capacity of VWF, together with the persistence of VWF propeptide. Paper-9787327.
These results indicate that, at moderately high but not very high shear rates, fibronectin assembly in platelet aggregates that form in response to collagen enhances thrombus formation and serves as an alternative to VWF-mediated enhancement. Paper-12237487.
Porcine VWF induced p38 MAPK activation by 1 min post-addition; assessed by phosphorylation of a recombinant p38 MAPK fusion protein substrate termed glutathione S-transferase- MAPK activated protein kinase-2. Paper-2074401.
Plasma levels of tissue plasminogen activator/ plasminogen activator inhibitor-1 complex and von Willebrand factor are significant risk markers for recurrent myocardial infarction in the Stockholm Heart Epidemiology Program (SHEEP) study. Paper-8371709.
Although the release of both factors appears to be regulated similarly, they exhibit opposing physiological effects in the vasculature with vWF inducing coagulation and platelet aggregation and tPA triggering fibrinolysis and thrombolysis. Paper-9243449.
In contrast, the receptor function of GP Ib exhibited restricted species specificity, since only the chimeric complex containing human GP Ib alpha bound human von Willebrand factor and supported platelet aggregation mediated by ristocetin. Paper-87197.
We examined the hypothesis that filamin A binding to the cytoplasmic tail of platelet glycoprotein Ibalpha ( GpIbalpha) is regulated by pathologic shear stress and modulates von Willebrand factor (VWF)-induced platelet activation. Paper-10000356.
von Willebrand factor ( VWF) protects factor VIII ( FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall, thus playing an important role in hemostasis and thrombosis. Paper-13141968.
Furthermore, the results suggest either that patients with VWd have a double defect in VWF and tissue plasminogen activator or that the primary deficiency of VWF influences the synthesis and/or release of t-PA by endothelial cells. Paper-11730190.
This loss could not be accounted for by modification of FVIII/ vWF by thrombin or platelet enzymes since no effect of thrombin on the multimeric structure of FVIII/ vWF in the absence of platelets or in the presence of platelet lysates was observed. Paper-4064938.
Von Willebrand factor ( VWF) is unable to interact spontaneously with platelets because this interaction requires a conversion of the VWF A1 domain into a glycoprotein Ibalpha ( GpIbalpha) binding conformation. Paper-11216503.
It did not significantly inhibit isolated GPIIb/IIIa binding to immobilized von Willebrand Factor. At low doses (1.5-3.0 micrograms/mouse), decorsin protected mice against death from pulmonary thromboembolism, showing an effect similar to eristostatin. Paper-522319.
Most cases in adults are caused by acquired autoantibodies that inhibit ADAMTS13, a metalloprotease that cleaves von Willebrand factor within nascent platelet-rich thrombi to prevent hemolysis, thrombocytopenia, and tissue infarction. Paper-12848624.
BACKGROUND: Functional deficiency of ADAMTS13 in thrombotic thrombocytopenic purpura (TTP) patients is associated with circulating ultralarge von Willebrand factor ( VWF) molecules that display spontaneous platelet-binding capacities. Paper-13854030.
The presence of the ABO blood group has a significant influence on vWF:Ag values; individuals with blood group O had the lowest mean vWF:Ag level (74.8 U/dL), followed by group A (105.9 U/dL), then group B (116.9 U/dL), and finally group AB (123.3 U/dL). Paper-5719424.
Monoclonal antibodies against the vWf binding site on GPIb (6D1) and the vWf and fibrinogen binding sites on GPIIb/IIIa (LJP5 and LJ-CP8, respectively) were used to characterize the mechanism of vWf binding to stimulated platelets. Paper-5566356.
In addition, cell proliferation and vWF expression was stimulated by VEGF, and the endothelial cell adhesion molecules CD54 ( ICAM-1), and CD106 ( VCAM-1) became transiently inducible by tumor necrosis factor-alpha ( TNF-alpha). Paper-8652196.
In this study, we showed that VEGF receptor-2 ( VEGFR2), but not VEGFR1, is responsible for VEGF- induced release of von Willebrand factor ( vWF), a major marker of WPBs. Paper-13948000.
The monoclonal antibody CLB-RAg 201 inhibited the binding of FVIII- VWF to purified vessel wall collagen type I and III and all platelet adherence to collagen type III and the platelet adherence to subendothelium that was mediated by FVIII- VWF in plasma. Paper-4819406.
Binding of VWF in solution to immobilized A/C was inhibited by ristocetin and preincubation of platelets with A/C abolished ristocetin/ VWF-induced platelet aggregation, indicating that the interaction of A/C with VWF is mediated by the VWA1 domain. Paper-13336200.
We further conclude that VWF- induced platelet aggregation does not directly depend on Erk activation but has an absolute requirement for Src/ Erk- mediated TXA2 generation. Paper-10977659.
Desmopressin shortened postoperative bleeding time, gave an early FVIII/ vWF complex increase, prevented antithrombin III from falling to critically low values and appeared to activate the fibrinolytic system, both by tPA increase and PAI-1 decrease. Paper-7096891.
In this study we investigated mechanisms of platelet interaction with von Willebrand factor ( vWF) induced by activating anti-glycoprotein (GP)IIb-IIIa antibody CRC54 directed against LIBS (ligand- induced binding site epitope) in GPIIIa. Paper-10879588.
While the roles that leucine tandem repeats may normally play within the GPIb/IX complex are not yet known, the perturbation of such a repeat in GPIb alpha may impair interaction with other components of the complex and/or with the binding of vWF. Paper-49813.
Our results indicate that the essential regions for the binding of APC and VWF to FVIII overlap and that the protective effect of VWF on APC- catalyzed FVIII inactivation includes competitive inhibition of APC binding to FVIII by VWF. Paper-9459708.
The absence of the leucine 179 in a patient's GPIb alpha is believed to cause a conformational change in the protein which would account for the lack of binding of most of the MoAbs tested and would be responsible for the absence of von Willebrand factor binding. Paper-174735.
VWF- induced Erk2 phosphorylation and thromboxane A2 ( TXA2) release were completely blocked by PP2, an Src family kinase inhibitor, suggesting that Erk is downstream of Src family kinases. Paper-10977659.
In this study, we investigated whether ABO groups affect VWF survival by monitoring the post-DDAVP time courses of VWF antigen (VWF:Ag), VWF collagen binding (VWF:CB) and factor VIII ( FVIII) in 47 healthy subjects (28 O and 19 non-O blood groups). Paper-12770784.
In addition, platelet adhesion to a VWF-coated surface was decreased by 50% in the presence of beta(2) GPI (P < .03). beta(2) GPI binds to the A1 domain of VWF but preferably when the A1 domain is in its active glycoprotein Ibalpha-binding conformation. Paper-13400028.
A 2-h incubation of human umbilical vein endothelial cells with oncostatin M increases thrombin- induced secretion of vWf to the same extent as tumour necrosis factor-alpha or interleukin-1 (137+/-26% of control for 5 ng/ml oncostatin M, P < 0.001, n=5). Paper-1738825.
Elastase and proteinase 3 ( PR3) cleave multimeric VWF and FRETS-VWF73 at the V(1607)-T(1608) peptide bond; cathepsin G and matrix metalloprotease 9 cleave VWF substrates at the Y(1605)-M(1606) and M(1606)-V(1607) bonds, respectively. Paper-13943275.
The inability of PC2 and PC3 to cleave vWF was apparently not due to the absence of a transmembrane domain, since deletion of the transmembrane domain from PACE resulted in a secreted form which retained its propeptide processing activity within the secretory apparatus. Paper-58808.
Glycoprotein ( GP) Ibalpha of the GPIb-IX-V complex and GPVI bind von Willebrand factor ( vWF) and collagen, respectively, and are critical for the initial interaction of circulating platelets with the injured vessel wall under high shear conditions. Paper-10604288.
Fibrinogen and vWF dependent platelet aggregation was completely suppressed by GP IIb-IIIa antagonists--preparations Monafram (F(ab')2 fragments of monoAB that blocked GP IIb-IIIa receptor activity) and aggrastat (RGD-like peptidomimetic). Paper-11521155.
Thrombotic thrombocytopenic purpura (TTP) is often associated with acquired or congenital deficiency of the von Willebrand factor- cleaving metalloprotease, ADMATS13 (Lammle B et al., J Thromb Haemost 2005;3:1663-1675; Schneppenheim et al., Blood 2003;101:1845-1850). Paper-12954581.
Autoimmune inhibitors or genetic mutations of a von Willebrand factor ( VWF) cleaving metalloprotease ( ADAMTS13) leads to the accumulation of unusually large multimeric forms of VWF in TTP, facilitating adherence of platelets and development of microthrombi. Paper-13440942.
Aggregation supported by vWF unlike fibrinogen supported aggregation was almost completely inhibited not only by GPIIb-IIIa antagonists (F(ab')2 fragment of blocking anti-GPIIb-IIIa antibody CRC64 and peptidomimetic aggrastat) but also by anti-GPIb blocking antibody AK2. Paper-10879588.
A severe deficiency in von Willebrand factor- cleaving protease ( ADAMTS13) activity (< 5% that in normal plasma) has been observed in most patients with a diagnosis of thrombotic thrombocytopenic purpura (TTP) but not in those with a diagnosis of hemolytic uremic syndrome. Paper-9186520.
RESULTS: Our data demonstrate that botrocetin/ VWF/GPIbalpha- mediated agglutination results in calcium-independent protein kinase C (PKC) and phospholipase A2 ( PLA2) activities required for GPIbalpha-elicited TXA2 production that in turn causes dense granule secretion. Paper-10911625.
However, 2% MyHC+ cells in E2.5-E3 hearts and 0.3% in E4-E6 hearts, also express vWF/Flk-1; and when cultured 3 days, >40% of the MyHC+ cells express vWF/Flk-1, but they do not express Vezf1, vascular endothelial cadherin, or Tie2. Paper-13416959.
The infusions of saline or DDAVP after cryoprecipitate did not further increase FVIII and vWF plasma levels and had no effect on the plasma levels of tissue plasminogen activator ( tPA), which are raised by DDAVP in normal subjects and in patients with vWD of other types. Paper-8248735.
To define the functional role of these three residues, we have introduced selected mutations in a soluble recombinant GP Ib alpha fragment (corresponding to the sequence 1-302 of the mature protein) that binds vWF and alpha-thrombin with the same attributes as intact GP Ib-IX-V complex. Paper-206743.
Growth factors are strongly linked to smooth muscle cell proliferation that contributes significantly to the vascular occlusive process and it has been shown that vascular endothelial cell growth factor ( VEGF) stimulates release of vWF from endothelial cells. Paper-2163850.
These data indicate that two soluble fragments of human GP Ib alpha with binding activity for vWF and thrombin can be expressed in mammalian cells and that the incorporation of GP Ib alpha into the surface membrane does not depend on co-expression with GP Ib beta and/or GP IX. Paper-100135.
Mixing experiments demonstrated an inhibitory effect of uremic plasma on SIPA of normal platelets (decreased from 39% +/- 3% at baseline to 31% +/- 3% after incubation in uremic plasma) along with an activation-independent increase in platelet- bound fibrinogen and platelet- bound vWF. Paper-518149.
Incubation with dibutyryl-cAMP and RA stimulated the expression of the EPC differentiation markers von Willebrand Factor ( vWF) and VEGF receptor 2 (VEGFR-2), indicating successful differentiation in the fibrin clot. Paper-13848887.
We found that cultured human microvascular endothelial cells from the intestine (HIMEC) and from nasal polyps (PMEC), but not human umbilical vein endothelial cells (HUVEC), contained IL-8 in intracellular granules that coexpressed von Willebrand factor ( vWf ). Paper-1646712.
Neutrophil cathepsin G modulates the platelet surface expression of the glycoprotein ( GP) Ib-IX complex by proteolysis of the von Willebrand factor binding site on GPIb alpha and by a cytoskeletal-mediated redistribution of the remainder of the complex. Paper-125179.
The monoclonal antibody 31H3 against D' domain of vWF (epitope aa 66-76) that partially inhibits the FVIII binding and recognizes only nonreduced vWF, showed a decreased ability to bind Asn116rvWF when used as capture-antibody in enzyme-linked immunosorbent assay ( ELISA). Paper-1707918.
Physical conditioning resulted in a more pronounced increase in von Willebrand factor ( vWF) and factor VIII clotting activity (FVIII:c) in Cat I and II and a more pronounced shortening of the activated partial thromboplastin time in all categories at maximal exertion and during recovery. Paper-8447962.
The vWF- stimulated cytoskeletal association of PtdIns 3-kinase and pp60c-src required platelet stirring and aggregation, was specifically blocked by an anti-GPIb monoclonal antibody, and was not observed in platelets lacking the glycoprotein Ib/IX complex ( Bernard-Soulier syndrome). Paper-136378.
Glycoprotein Ibalpha contains a binding site for von Willebrand factor through which it mediates platelet adhesion; GP V is required for the complex to bind thrombin with high affinity; and both GP Ibbeta and GP IX are necessary for efficient plasma membrane expression of the complex. Paper-1654917.
Maternal sera with anti-HPA-1a antibodies affected neither the EC expression of intracellular adhesion molecule-1 ( ICAM-1), vascular adhesion molecule-1 ( VCAM-1) and tissue factor ( TF) nor the release of van Willebrand factor ( vWF) or interleukin (IL)-8 nor the integrity of ECs. Paper-10450268.
Functional characteristics, including vWF release upon histamine stimulation and upregulated expression of VEGF and VEGF type 1 receptor in response to hypoxia, were indistinguishable between the MOMC-derived endothelial-like cells and cultured mature endothelial cells. Paper-12343774.
Patients with extra-articular disease had a significant increase in PAI-1 activity and reduced tPA release in the venous occlusion test. von Willebrand factor, PAI-1 and also haptoglobin and triglycerides were significantly increased in the group of patients who later suffered from TE. Paper-7876697.
Mocarhagin, a novel cobra venom metalloproteinase, cleaves the platelet von Willebrand factor receptor glycoprotein Ibalpha. Identification of the sulfated tyrosine/anionic sequence Tyr-276-Glu-282 of glycoprotein Ibalpha as a binding site for von Willebrand factor and alpha-thrombin. Paper-577446.
We conclude that in a shear field, soluble or local platelet-released TSP-1 can protect unfolded endothelium- bound and subendothelial VWF from degradation by plasma ADAMTS13, thus securing platelet tethering and thrombus adherence to inflamed and injured endothelium, respectively. Paper-10815654.
Vascular Endothelial Growth Factor (VEGF) Receptor-2 Tyrosine 1175 Signaling Controls VEGF- induced von Willebrand Factor Release from Endothelial Cells via Phospholipase C-{gamma}1- and Protein Kinase A-dependent Pathways. Paper-13948000.
CONCLUSIONS: G894T polymorphism on the eNOS gene increases the risk for premature MI and modifies the response of vascular endothelium during the acute phase of MI by affecting the release of vWF, IL-6, and oxidative stress status, an effect diminished one year after the event. Paper-11099550.
Inhibition of p38 MAPK had no effect on VWF-induced platelet alpha or lysozomal granule release, expression of activated GPIIb IIIa, modulation of membrane glycoprotein CD41, expression of phosphatidylserine as assessed by annexin V binding, microparticle formation, or platelet agglutination. Paper-2074401.
These data indicate that shear-induced VWF binding to platelet GpIb-IX-V activates Pyk2, ERK1/2, p38, and cPLA2, but that the magnitude of these responses is below the threshold needed to enhance shear-induced VWF-dependent platelet aggregation in the presence of plasma. Paper-10639810.
We investigated changes in plasma vWF:Ag and TM antigen levels during the course of regular hemodialysis treatment ( RDT) in 14 patients undergoing RDT in order to evaluate the effect of hemodialysis (HD) on endothelial cells. vWF:Ag and TM were both measured by the sandwich EIA method. Paper-6503833.
INTRODUCTION: The purpose of this study was to assess the requirement for the RGD sequence of von Willebrand factor ( VWF) for its binding to the beta3 chain of integrins and the structural basis for the specificity of monoclonal antibody (MoAb) 9 which specifically binds to VWF and inhibits this interaction. Paper-10712994.
A dominant-negative mutant of p38, p38AF, inhibits alphaIIb beta3 activation induced by VWF binding to its receptor, the platelet glycoprotein Ib-IX (GPIb-IX), and p38 inhibitors diminish platelet aggregation induced by VWF or low-dose thrombin. Paper-10815678.
Using monoclonal antibodies (MoAbs) against the platelet glycoproteins (GP) IIb/IIIa and Ib (MoAbs 10E5 and 6D1, respectively), we demonstrated that the ADP-induced increase in platelet- vWF expression on control platelets primarily involved the binding of secreted platelet- vWF to the platelet GPIIb/IIIa. Paper-6195850.
Deletion and substitution variants of FVIII as well as the precise epitope mapping of FVIII antibodies which inhibit the procoagulant function of the protein or its binding to von Willebrand factor have provided insight into the identification of regions of FVIII which are required for normal function. Paper-6167267.
We tested the hypothesis that DDAVP induces vWF secretion by binding to V2R and activating cAMP- mediated signaling in endothelial cells. vWF secretion from human umbilical vein endothelial cells (HUVECs) can be mediated by cAMP, but DDAVP is ineffective, presumably due to the absence of V2R. Paper-8393968.
A disintegrin-like and metalloprotease with thrombospondin type 1-motif 13 ( ADAMTS-13) cleaves the A2 domain of von Willebrand factor ( VWF), converting the ultralarge (UL) and hyperactive VWF multimers freshly released from endothelial cells to smaller and less active forms found in plasma. Paper-10752259.
Raised levels of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate, as well as membrane-permeable calcium chelators, inhibited these [Ca(++)](i) oscillations and prevented stable adhesion without affecting the dynamic characteristics of the typical platelet translocation on VWF mediated by GPIbalpha. Paper-9574246.
Whether the down-regulation of CD34 correlates with an age- associated reduction of the angiogenetic properties of EC or an age-related over-expression of vWf as a relevant cofactor for the raised coagulatory activity and the increase in thrombotic diseases resp coronary heart disease in older patients, remains subject to debate. Paper-9200016.
This type of HUS is characterized by obstruction of the glomeruli and renal microvasculature by platelet-fibrin thrombi, acute renal failure, thrombocytopenia, microvascular hemolytic anemia, and plasma levels of von Willebrand factor (VWF)- cleaving protease ( ADAMTS13) activity that are within a broad normal range. Paper-11522707.
Pretreatment of normal platelets with 5 mM EDTA (37 degrees C for 90 min) or RGDS (2 mM), which disrupts the binding of various adhesive proteins to platelet integrins and inhibits fibrinogen-mediated platelet aggregation, did not alter the vWF- stimulated activation and cytoskeletal association of PtdIns 3-kinase and pp60c-src. Paper-136378.
In addition to its interaction with vWF, we show that OPG also binds with high avidity to the vWF reductase, thrombospondin ( TSP-1), raising the intriguing possibility that OPG may provide a link between TSP-1 and vWF. Paper-10732848.
In contrast, neither appearance nor exocytosis of tPA storage granules is affected. siRNA- mediated downregulation of annexin A2/ S100A10 and disruption of the complex by microinjection of peptide competitors result in a marked reduction in vWF but not tPA secretion, without affecting the appearance of WPbs. Paper-10486596.
Other authors [Haverstick et al. (1985) Blood 66, 946-952; Ginsberg et al. (1985) J. Biol. Chem. 260, 4133-4138] have shown that a tetrapeptide, Arg-Gly-Asp-Ser, inhibited the binding of fibrinogen, fibronectin, and von Willebrand factor ( vWf) to stimulated platelets and that fibrinogen competes with vWf and fibronectin for binding. Paper-5149311.
METHODS: Isolated AVM brain endothelial cells and control brain endothelial cells were evaluated immunohistochemically for expression of the endothelial cell markers von Willebrand factor and CD31, as well as angiogenic factors including vascular endothelial growth factor A, interleukin-8, and endothelin-1. Paper-13576378.
An anionic/sulfated tyrosine sequence of the GP Ib alpha-chain that is critical for binding of the GP Ib-IX-V complex to both vWF and alpha-thrombin is analogous to sulfated anionic amino acid sequences mediating interactions of other adhesive proteins, including P-selectin binding to PSGL-1 and Factor VIII binding to vWF. Paper-961979.
On average, type 1 VWD plasma was misidentified as type 2 VWD plasma in 11% of cases, and laboratories that performed the ristocetin cofactor assay for von Willebrand factor ( VWF:RCo) without performing the collagen- binding activity assay for VWF (VWF:CB) were 6 times more likely to make such an error than those that did perform the VWF:CB. Paper-11001899.
BACKGROUND: Severe deficiency of von Willebrand factor- cleaving protease ( ADAMTS-13) activity (<5% of normal) is specific for classical thrombotic thrombocytopenic purpura (TTP), a disorder presenting with thrombocytopenia, microangiopathic haemolytic anaemia and often with organ dysfunction such as neurological symptoms, renal failure, and fever. Paper-9946475.
Substitution of His86 with either Ala or Glu resulted in a gain of VWF- binding function as judged by increased VWF binding in the presence of the modulators ristocetin and botrocetin and by enhanced adhesion of Chinese hamster ovary (CHO) cells expressing the mutant GP Ibalpha to immobilized VWF under conditions of flow. Paper-11068117.
These synonyms are used for gene VWF (von Willebrand factor): vWF, VWD, F8VWF.
These accession numbers are used for gene VWF: Q99806 (UNIPROT__AC), CAA26503 (NCBI_GENBANK__AC), B4DMS3 (UNIPROT__AC), AAB39987 (NCBI_GENBANK__AC).
VWF is a homologue of VWF (von Willebrand factor) from Bos taurus.
VWF is a homologue of VWF (von Willebrand factor) from Pan troglodytes.
VWF is a homologue of VWF (von Willebrand factor) from Gallus gallus.
VWF is a homologue of VWF (von Willebrand factor) from Canis lupus familiaris.
VWF is a homologue of Vwf (Von Willebrand factor homolog) from Mus musculus.
VWF is a homologue of Vwf (Von Willebrand factor homolog) from Rattus norvegicus.
Important links !
iHOP - Information Hyperlinked over Proteins .
Concept & Implementation by Robert Hoffmann.