The most recent information on VWF is here. 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. The two bands also reacted with anti- alpha 2M and anti- vWF antibodies. Paper-7882172. Coagulation tests showed abnormalities in FXIII subunits and FVIII/ vWF complex. Paper-6532249. These conditions would allow VWF to act as a cargo targeting OPG to WPBs. Paper-13409384. Identification of ADAMTS13 peptide sequences binding to von Willebrand factor. Paper-14220794. ADAMTS13 regulates the multimeric size of von Willebrand factor ( VWF). Paper-13513987. We observed positive associations between changes in IL-6, VWF, MCP-1, and CRP. Paper-14437735. The rise in vWF is associated with that in CRP and with enhanced platelet reactivity. Paper-10692041. CONCLUSIONS: VWF has an inhibitory effect on the measurement of FVIII clotting activity. Paper-13498785. Structures of glycoprotein Ibalpha and its complex with von Willebrand factor A1 domain. Paper-9535489. Platelet- VWF complexes are preferred substrates of ADAMTS13 under fluid shear stress. Paper-12682861. IL-8 correlated positively with both TNF-alpha and vWF in the entire study group. Paper-9600581. Therefore, the spacer domain is required for ADAMTS13 binding to von Willebrand factor. Paper-10742577. An AC reduces post-exercise vWf:Ag and tPA antigen without affecting tPA or PAI-1 activity. Paper-10498675. The ERK2 activity required for platelet adhesion was dependent on the interaction of vWF with GPIb. Paper-11135107. Shear-induced von Willebrand factor- mediated platelet surface translocation of the CD40 ligand. Paper-10688623. The LPL mass was inversely correlated with plasma vWF level at a high correlation coefficient value. Paper-1680628. ADAMTS13 is a metalloproteinase that cleaves von Willebrand factor ( VWF) multimers. Paper-10826395. Increasing levels of VWF were associated with a decrease in ADAMTS13 activity (r=-0.34; P=0.03). Paper-14297853. Fg caused a dose-dependent increase in ET-1 formation and release of vWF from the RHMECs. Paper-13694193. Antihemostatic activity of human granzyme B mediated by cleavage of von Willebrand factor. Paper-12903854. Echistatin inhibited ERK activation on vWF and vitronectin ( VN), but not albo B. Paper-10711994. Furthermore, vWF in solution at normal plasma levels also inhibited RBC adhesion to immobilized TSP. Paper-954197. ADAMTS-13 specifically cleaves a peptidyl bond between Y1605 and M1606 in the A2 domain of VWF. Paper-10204628. von Willebrand factor cleaved from endothelial cells by ADAMTS13 remains ultralarge in size. Paper-14011649. Here we present structures of the GpIbalpha amino-terminal domain and its complex with the VWF domain A1. Paper-9535489. Rab3D and annexin A2 play a role in regulated secretion of vWF, but not tPA, from endothelial cells. Paper-10486596. ADAMTS13 bound to endothelial cells exhibits enhanced cleavage of von Willebrand factor. Paper-14100800. Thrombospondin-1 and ADAMTS13 competitively bind to VWF A2 and A3 domains in vitro. Paper-15454502. CD133+ cells showed characteristics of endothelial-like cells by eNOS, CD141 and beginning vWF expression. Paper-12966690. CONCLUSIONS: Our observations demonstrate the existence of an interactive site for OPG within the VWF A1-domain. Paper-13409384. ADAMTS-13 metalloprotease interacts with the endothelial cell-derived ultra-large von Willebrand factor. Paper-9825860. WH2-22-1A also reduced the activity of plasma ADAMTS-13 to cleave large VWF multimers during perfusion. Paper-13538528. Von Willebrand factor targets IL-8 to Weibel-Palade bodies in an endothelial cell line. Paper-9756900. CONCLUSIONS: MMRN1 supports platelet adhesion by VWF-dependent and -independent mechanisms that vary by flow rate. Paper-13696408. However, little is known about changes of VWF associated with VWF-cleaving protease ( ADAMTS13) in AF. Paper-13733851. Oxidative modification of von Willebrand factor by neutrophil oxidants inhibits its cleavage by ADAMTS13. Paper-14096496. Efficiency of von Willebrand factor- mediated targeting of interleukin-8 into Weibel-Palade bodies. Paper-12619164. p38 MAPK is activated but not necessary in porcine von Willebrand factor-dependent platelet activation. Paper-2074401. VEGF and basic fibroblast growth factor can synergistically upregulate the vWF gene expression. Paper-10025929. Like the VWF regulatory proteinase ADAMTS-13, GrB- mediated cleavage is dependent upon VWF conformation. Paper-12903854. The inhibition of adhesion by vWF was shown to be the result of specific and saturable binding of vWF to TSP. Paper-954197. We observed that TSP1 partially blocked ADAMTS13 binding to A2 domain, A3 domain and full length VWF. Paper-15454502. High plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of VWF. Paper-14063774. How the different domains in ADAMTS13 control VWF proteolysis in vivo remains largely unidentified. Paper-15482872. In uncomplicated malaria VWF levels were also increased compared to healthy controls but ADAMTS13 activity was normal. Paper-14202883. METHODS: Immunoprecipiation of VWF- ADAMTS-13 complexes using anti- VWF antibodies and magnetic beads was used. Paper-14158764. CD34 was more sensitive and specific than vWf for staining endothelial cells associated with VEGF expression. Paper-8494246. P-selectin anchors newly released ultralarge von Willebrand factor multimers to the endothelial cell surface. Paper-10204678. These results indicate that TSP-1 regulates the multimeric size and therefore hemostatic activity of vWF. Paper-8993305. ADAMTS13 limits platelet-rich thrombosis by cleaving von Willebrand factor at the Tyr(1605)-Met(1606) bond. Paper-10803836. PAI-1, tPA, tPA/ PAI-1- complex and vWF were measured after two weeks, six and 12 months following randomisation. Paper-9383850. VWF reductase activity was present in the Ca(++)- binding repeats and C-terminal sequence of TSP-1, but not of TSP-2. Paper-9574251. In this work, we found that VWF stimulated the rapid and sustained phosphorylation of p38 MAP kinase (p38MAPK). Paper-10354047. ADAMTS13 gene inactivation upregulates release and intracellular VWF levels in E2-treated HUVEC. Paper-15616203. There was no clear influence of CRP on E-selectin, but 20 and 50 microg/ml CRP inhibited the release of vWF. Paper-9959012. Second, an anti- VWF antibody coimmunoprecipitates P-selectin from the histamine-activated endothelial cells. Paper-10204678. Transient binding of PMNs to VWF appeared to be mediated by P-selectin glycoprotein ligand-1 ( PSGL-1). Paper-12321403. FVIII, vWF and other factors related to thrombophilia were measured, ABO groups were analyzed by genotyping. Paper-11499745. ADAMTS13 cleaves multimeric von Willebrand factor ( VWF) to regulate VWF-mediated thrombus formation. Paper-14220794. Phospholipase D1 is specifically required for regulated secretion of von Willebrand factor from endothelial cells. Paper-13585621. METHODS AND RESULTS: In a solid-phase binding assay, VWF was able to bind specifically to OPG in a calcium-dependent manner. Paper-13409384. The proportion of TM-positive microvessels was expressed relative to total von Willebrand factor (vWF)-positive vessels. Paper-9546976. Effect of von Willebrand factor Y/ C1584 on in vivo protein level and function and interaction with ABO blood group. Paper-13226859. Thus, in addition to alphavbeta3, EC GP Ibalpha initiates ERK activation, and regulates ERK- induced EC migration on vWF. Paper-10711994. Alpha 2A adrenergic receptor polymorphism is associated with plasma von Willebrand factor levels in a general population. Paper-12876710. Levels of ECM- associated von Willebrand factor ( vWF) and fibronectin ( FN) were also quantified ( ELISA). Paper-6926198. CONCLUSIONS: Our findings demonstrate that FVIII trafficking to WPBs is independent of Tyr1680 and high-affinity binding to VWF. Paper-12532545. Interaction of TSP-1 with vWF is mediated by TSP-1 type 1 properdin domains and the vWF A3 domain. Paper-8993305. In HUVEC, OPG co-localizes with P-selectin and von Willebrand factor ( vWF), within the Weibel-Palade bodies (WPB). Paper-10732848. ADAMTS13 in cell lysate or serum-free conditioned medium cleaved von Willebrand factor ( VWF) specifically. Paper-12237484. The ability of FVIII to enhance VWF cleavage by ADAMTS13 is rapidly lost after pretreatment of FVIII with thrombin. Paper-14328179. Moreover, recombinant PSGL-1 protein and cell surface- expressed PSGL-1 directly interacted with VWF. Paper-12321403. These findings suggest that high purity VWF/ FVIII complex concentrates are effective in ITI, even in patients at high risk of failure. Paper-13326094. Functional variation in the arginine vasopressin 2 receptor as a modifier of human plasma von Willebrand factor levels. Paper-15191057. The plasma protein von Willebrand factor ( VWF) binds to FVIII and is known to be important for the functioning of FVIII. Paper-12831339. It was concluded that SB203580-inhibitable p38 MAPK activity induced by porcine VWF is not necessary for platelet activation. Paper-2074401. The distal carboxyterminal domains of murine ADAMTS13 influence proteolysis of platelet-decorated VWF strings in vivo. Paper-15482872. Understanding the role of von Willebrand factor and its cleaving protease ADAM TS13 in the pathophysiology of critical illness. Paper-13151312. P-selectin glycoprotein ligand 1 and beta2-integrins cooperate in the adhesion of leukocytes to von Willebrand factor. Paper-12321403. The expression of von Willebrand factor, soluble thrombomodulin, and soluble p-selectin during orthotopic liver transplantation. Paper-12453529. FVIII- LRP interaction involves the FVIII light chain, and FVIII- vWF complex formation plays a regulatory role in LRP binding. Paper-1964868. Arterial blood flow enhances glycoprotein Ibalpha ( GPIbalpha) binding to vWF, which initiates platelet adhesion to injured vessels. Paper-12927324. Discrepant activity levels of von Willebrand factor- cleaving protease ( ADAMTS-13) in congenital thrombotic thrombocytopenic purpura. Paper-10044104. ADAMTS13 is a plasma metalloprotease that cleaves ultralarge von Willebrand factor multimers to generate less thrombogenic fragments. Paper-14100800. Effect of genetic variations in syntaxin-binding protein-5 and syntaxin-2 on von Willebrand factor concentration and cardiovascular risk. Paper-15561480. mRNA levels of CD31, CD144, CD146 and von Willebrand factor do not serve as surrogate markers for circulating endothelial cells. Paper-15330009. Negative reactions were with cytokeratins, bcl-2, desmin, actin, VWF, S100, alpha-1-antitrypsin, CD99, lysozyme and FXIIIa. Paper-9567710. The metalloprotease ADAMTS-13 cleaves von Willebrand factor ( VWF) at the Y842/M843 peptide bond located in the A2 domain. Paper-10541414. These results indicate that shear-induced VWF binding to platelet GpIb-IX-V stimulates functionally important PI3-K activity. Paper-9877074. Effects of toll-like receptor-4 gene polymorphisms on soluble P-selectin and von Willebrand factor levels in hypercholesterolemic patients. Paper-12483103. Glycoprotein Ibalpha inhibitor complex structure reveals a combined steric and allosteric mechanism of von Willebrand factor antagonism. Paper-14166268. Plasma von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, and antithrombin III levels in Behçet's disease. Paper-522957. 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. Blood levels of vWf, VEGF, platelet count, C-reactive protein ( CRP), ceruloplasmin and carcinoembrionary antigen (CEA) were measured. Paper-10765411. The areas under the ROC curves were higher for IL-6 (0.72) than for the other variables (0.58 for F1 + 2, 0.52 for vWf and 0.54 for PAI-1). Paper-9405400. 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. The R273W mutation did not affect the ability of VWF to bind to BiP, Grp94, ERp72, calnexin, and calreticulin in COS-7 cells. Paper-8356667. INTRODUCTION: Deficiency of Von Willebrand factor (VWF)- cleaving protease ( ADAMTS13) causes platelet thrombosis in the microcirculation. Paper-15136206. ADAMTS13 specifically cleaves plasma von Willebrand factor ( VWF) and thereby controls VWF-mediated platelet thrombus formation. Paper-14578293. In an analogous murine model, FVIII/ vWF inhibitor plasma was obtained by immunizing goats with a purified human FVIII/ vWF complex. Paper-1027046. ADAMTS13 controls the multimeric size of circulating von Willebrand factor ( VWF) by cleaving the Tyr1605-Met1606 bond in theA2 domain. Paper-10839557. CONCLUSIONS: Our data demonstrate that the ADAMTS13 CUB and T2-8 domains influence proteolysis of platelet-decorated VWF strings in vivo. Paper-15482872. The ABO locus has functional effects on vWF and FVIII levels and is genetically correlated with FVIII, vWF and thrombosis. Paper-11499745. Binding of platelet glycoprotein Ibalpha to von Willebrand factor domain A1 stimulates the cleavage of the adjacent domain A2 by ADAMTS13. Paper-10362594. Recent advances have shown that TTP is caused by deficiency of a circulating, von Willebrand factor cleaving metalloprotease, ADAMTS13. Paper-13365300. IL-3 and TSF stimulated similar increases in vWF expression by human megakaryocytes contained in nonadherent bone marrow preparations. Paper-6868195. In conclusion, the alpha 2A adrenergic receptor 2372A/G polymorphism is associated with plasma von Willebrand factor levels in a general population. Paper-12876710. During differentiation, EPCs obviously lose CD133 and start to express CD31, vascular endothelial cadherin, and von Willebrand factor. Paper-9909255. The finding that an amino acid polymorphism in VWF may influence susceptibility to ADAMTS13 has potentially significant implications in diverse areas. Paper-10204643. 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. Monoclonal antibodies (MoAbs) 6D1 (anti-GPIb) and 328 (anti- VWF A1 domain), completely abolished SIPA and p125FAK phosphorylation mediated by 2B-rVWF. Paper-9728006. OBJECTIVES: We hypothesized that not all binding sites for ADAMTS-13 in VWF are cryptic and analyzed binding of native VWF to ADAMTS-13. Paper-14158764. 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. Confocal laser scanning microscopy was used to visualize coexpression of CD34, CD133, von Willebrand factor, or Pax7 on individual cells. Paper-12893261. Our findings suggest that FVIII and platelets are cofactors that regulate proteolysis of multimeric VWF by ADAMTS13 under physiological conditions. Paper-15341156. When the cells were cultured with 12-o-tetradecanoylphorbol-13-acetate (TPA), the expression of TSP was enhanced and vWF was also detected, but not Fbg. Paper-7873645. Furthermore, vWF binding to GPIb-IX induces phosphorylation of Thr-202/Tyr-204 of extracellular signal-regulated kinase 2 ( ERK2). Paper-9088534. When secretion was induced, OPG remained associated with VWF in extracellular patches of release under biochemical conditions found in blood plasma. Paper-13409384. We have investigated the role of p38 mitogen- activated protein kinase ( MAPK) in von Willebrand factor (VWF)-dependent platelet activation. Paper-2074401. Associations of IL-1 polymorphisms with the changes (Delta) in CRP, IL-1ra, E-selectin and vWF levels between 24 and 48 h were examined in later studies. Paper-9288348. Furthermore, recombinant ADAMTS13- mediated degradation of VWF multimers was entirely inhibited in the presence of plasma from a patient with acquired TTP. Paper-9331480. ATP augments von Willebrand factor-dependent shear- induced platelet aggregation through Ca2+-calmodulin and myosin light chain kinase activation. Paper-10309910. The present case of lymphangioma showed strong immunohistochemical reactivity of angiogenin and vWF, while it showed weak reactions of VEGF and PCNA. Paper-9215689. An autoantibody epitope comprising residues R660, Y661, and Y665 in the ADAMTS13 spacer domain identifies a binding site for the A2 domain of VWF. Paper-14180437. ETP in PRP, platelet-derived procoagulant activity and vWF were correlated and higher in patients than in controls (p=0.002, p=0.045 and p=0.0006, respectively). Paper-9945507. 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. 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. Filamin A binding to the cytoplasmic tail of glycoprotein Ibalpha regulates von Willebrand factor-induced platelet activation. Paper-10000356. INTRODUCTION: ADAMTS13 (a disintegrin-like and metalloprotease with thrombospondin type 1 repeat motif. 13) is the major metalloprotease for VWF degradation. Paper-15454502. 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. TM levels were found to be increased both before and after therapies whereas HCFII and vWF levels were not different from those of the control group. Paper-1857269. Serum HGF, nitric oxide (NO), plasma von Willebrand factor ( vWF), and endothelin (ET) were measured before treatment and after 8 weeks of treatment. Paper-15368747. 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. 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. 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. Constitutive ADAMTS-13 released from endothelial cells may contribute to the maintenance of cell surfaces free of hyperadhesive VWF multimeric strings. Paper-14602459. RESULTS: Co-immunoprecipitation demonstrated that ADAMTS-13 binds to native multimeric VWF (K(d) of 79 +/- 11 nmol L(-1)) with no measurable proteolysis. Paper-14158764. The absorption of FVIII/ VWF to collagens was affected by ionic concentration and FVIII/ VWF was only totally bound at relatively low ionic strength. Paper-4501300. GrB delays ristocetin- induced platelet aggregation and inhibits platelet adhesion and spreading on immobilized VWF under static conditions. Paper-12903854. In vitro, GrB cannot cleave the VWF conformer found in solution, but cleavage is induced when VWF is artificially unfolded or presented as a matrix. Paper-12903854. 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 mechanism of the protective effects of E2 on the cardiovascular system could be explained by the intracellular regulation of VWF produced by ADAMTS13. Paper-15616203. However, the mutated ADAMTS-13 bound to VWF substrate similarly as the wild-type metalloprotease and remained active in cleaving (UL)VWF under flow conditions. Paper-13888266. Whether the proteins were first combined in solution or sequentially applied to the slide, the presence of vWF inhibited the binding of sickle RBC to TSP. Paper-954197. Genetic polymorphisms G894T on the eNOS gene is associated with endothelial function and vWF levels in premature myocardial infarction survivors. Paper-10566647. It was reported that TSP1 might protected VWF from cleaving by ADAMTS13, yet the underlying mechanism of this VWF protection has remained unknown. Paper-15454502. 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. In this study, the histological type of F6 cells was investigated by immunohistochemistry with specific markers: vimentin, CD117, desmin, NSE and vWF. Paper-12252741. BACKGROUND: Vascular endothelial growth factor ( VEGF) and histamine induce von Willebrand factor ( VWF) release from vascular endothelial cells. Paper-14338671. CONCLUSIONS: Genetic variability in STXBP5 and STX2 affects both VWF concentration and activity in young individuals with premature arterial thrombosis. Paper-15561480. Von Willebrand factor- cleaving protease ( ADAMTS-13) activity in thrombotic microangiopathies: diagnostic experience 2001/2002 of a single research laboratory. Paper-9946475. ADAMTS13 metalloprotease regulates the multimeric size of von Willebrand factor ( VWF) by cleaving the Tyr1605-Met1606 bond in the VWF A2 domain. Paper-14010442. We have recently found that beta2-glycoprotein I is able to inhibit platelet binding to VWF, indicating a role in the pathophysiology of arterial thrombosis. Paper-14063774. ADAMTS13 could cleave approximately 14% of VWF pretreated with guanidine HCl, suggesting that this substrate is heterogeneous in susceptibility to proteolysis. Paper-10826395. In the present study, we expressed different C-terminal domain VWF fragments and evaluated their binding to ADAMTS13 and its truncated mutants, MDTCS and del(TSP5-CUB). Paper-14010442. 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. Recombinant erythropoietin ( EPO) and human interleukin 6 ( IL-6) each induced a twofold increase in vWF, and each acted additively with 10 U/ml IL-3. Paper-6868195. This increased risk is attributable to the fact that ABO blood group influences plasma levels of a coagulation glycoprotein named von Willebrand factor ( VWF). Paper-14709865. Conversely to CD31 and vWF, a marked increase in glomerular reactivity for TM was observed in all the patients with GN (GN: 2.12 +/- 0.32, NK: 0.95 +/- 0.05, p < 0.02). Paper-10904525. Production, crystallization and preliminary crystallographic analysis of an exosite-containing fragment of human von Willebrand factor- cleaving proteinase ADAMTS13. Paper-13869546. Kinetic analysis of VWF115 carrying the D1614A mutation suggested that Arg349 in the ADAMTS13 disintegrin-like domain interacts directly with Asp1614 in VWF A2. Paper-13810718. 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. Leucine-rich repeats 2-4 (Leu60-Glu128) of platelet glycoprotein Ibalpha regulate shear-dependent cell adhesion to von Willebrand factor. Paper-12209319. Glycoprotein (GP) Ibalpha, a member of the leucine-rich repeat ( LRR) protein family, mediates platelet adhesion to immobilized von Willebrand factor ( VWF). Paper-11068117. BACKGROUND: ADAMTS13 cleaves ultralarge von Willebrand factor ( VWF) and plays a significant role in vascular biology and thrombotic thrombocytopenic purpura. Paper-13733892. Theoretically, von Willebrand factor ( VWF) should be capable of binding all factor VIII ( FVIII), but an unbound FVIII (uFVIII) plasma fraction remains. Paper-10467367. 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. Successful treatment of a young infant who developed high-titer inhibitors against VWF- cleaving protease ( ADAMTS-13): important discrimination from Upshaw-Schulman syndrome. Paper-9243399. 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. We conclude that R763G is a new type 2N VWD mutation located in the VWF propeptide which alters the proteolytic processing of VWF and consequently its binding to FVIII. Paper-12210309. Thus we found no evidence that vWF is necessary for AHF to function in the coagulation of recalcified kaolin- activated vWF-deficient platelet-rich plasma. Paper-4535849. Osteoprotegerin ( OPG) is localized to the Weibel-Palade bodies of human vascular endothelial cells and is physically associated with von Willebrand factor. Paper-10732848. For identification of EPC and OEC, RT-PCR was performed for each specific cell markers, such as AC133, CD45, CXCR4, CDH5, vWF, eNOs, CD34, and Flt 1. Paper-12843256. Maximum parsimony, maximum likelihood, and Bayesian methods were used to analyze sequence data obtained from protein-coding portions of ApoB, BRCA1, IRBP, Rag1, and vWF. Paper-13761437. Highly purified FVIII products thus appear to be suitable for achieving immune tolerance without negative effects on endogenous von Willebrand factor levels and activity. Paper-8275977. Recombinant pieces of TSP-1 and TSP-2 incorporating combinations of domains that span the entire subunit were produced in insect cells and examined for VWF reductase activity. Paper-9574251. ADAMTS-13 cleaves long von Willebrand factor multimeric strings anchored to endothelial cells in the absence of flow, platelets or conformation-altering chemicals. Paper-13498786. In contrast, the attachment to WT- vWF of HUVEC, treated with TNF-alpha + IFN-gamma was completely inhibited by vWF-A1 and inhibited only 35% by the anti-VNR antibody LM609. Paper-1024407. Consequently, the percentage of VWF strings cleaved by ADAMTS-13 at VWF Y(1605)-M(1606) decreased as the rate of VWF string secretion was increased by cell stimulation. Paper-14602459. These results suggest that the combination of vWF multimeric analysis and the radiomonoclonal- labeled vWF method may be very useful in the assessment of AHF preparations. Paper-5784819. 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. This mutation prevents FVIII binding to a human monoclonal antibody recognizing the C2 domain and inhibiting FVIII binding to VWF and phospholipids. Paper-10214903. Fibronectin and 130-kDa molecule complex mimics snake venom botrocetin-like structure potentially modulating association between von Willebrand factor and vascular vessel wall. Paper-289081. We conclude that in type 2B vWD, prolonged lifetimes of vWF bonds with GPIbalpha on circulating platelets may allow ADAMTS-13 to deplete large vWF multimers, causing bleeding. Paper-12927324. The heterogeneity regarding the presence or absence of vWF protease activity in patients with TTP/ HUS was confirmed by finding a low negative predictive value of 0.50 with the CBA. Paper-9629638. The interaction of von Willebrand factor with specific ADAMTS13 domains was characterized with a binding assay employing von Willebrand factor immobilized on a plastic surface. Paper-10742577. We propose that this novel VWF C-terminal binding site may participate as the initial step of a multistep interaction ultimately leading to proteolysis of VWF by ADAMTS13. Paper-14010442. 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. 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. All the newly formed vessels were positive for endothelial cell markers ( CD31, CD34, von Willebrand factor) and negative for markers of lymphatic vessels ( podoplanin). Paper-12850333. 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. BACKGROUND: The multidomain metalloprotease ADAMTS13 regulates the size of von Willebrand factor ( VWF) multimers upon their release from endothelial cells. Paper-15482872. INTRODUCTION: Upon stimulation, endothelial cells release von Willebrand factor ( VWF) in the unusually large (UL) and hyperactive forms that are rapidly cleaved by ADAMTS-13. Paper-13888266. In the diabetes mellitus along with PAOD group, VWF antigen was significantly higher, but ADAMTS13 antigen or activity did not differ significantly from those of healthy controls. Paper-14095512. In in vitro studies, VWF has been shown to inhibit both the uptake of FVIII by immature dendritic cells and the activation of FVIII-specificT-cells in a dose-dependent manner. Paper-12831339. 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. 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. In patients with liver cirrhosis hepatic FVIII and LRP mRNA levels were significantly lower than controls (p < or = 0.010), while VWF mRNA was significantly higher (p < or = 0.050). Paper-10435832. Analogous to VWF-platelet interaction, VWF provided binding sites for leukocyte receptors involved in rolling ( PSGL-1) and stable (beta2-integrins) adhesion. Paper-12321403. Expression of EPCR, TM, and vWF was analyzed via quantitative confocal immunofluorescence in residual saphenous veins collected following coronary artery bypass procedures. Paper-15675926. In 51 patients not treated with recombinant EPO, serum levels of this hormone inversely correlated with whole blood RIPA, AT, age, vWF antigen, AGP, and positively with viral hepatitis marker. Paper-9285575. 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. The low levels of FVIII observed in the absence of vWF are due to an enhanced clearance of FVIII by binding to LRP and removal from the circulation through endocytosis. Paper-9328110. Plasma immunoreactive TM, vWF, PAI-1, ICAM-1, E-selectin, and PF 1+2 were measured before the randomization procedure and after 12 weeks, at the start, after 10 and 180 minutes of HD. Paper-13578922. The vWF domain for binding to FVIII was assayed by a method previously described but using recombinant FVIII (r- FVIII, Kogenate), which contains no vWF, instead of Hemofil M (HM). Paper-1225270. Long-term expression of von Willebrand Factor by a VSV-G pseudotyped lentivirus enhances the functional activity of secreted B-Domain- deleted Coagulation Factor VIII. Paper-12489879. This could be distinguished from aquaporin 2 (AQP2)-dependent NDI by the response of factor VIII and von Willebrand factor ( vWF) to 1-deamino-8-D-arginine vasopressin (DDAVP) administration. Paper-10181481. Moreover, results with ADAMTS-13 deletion mutants indicated that binding to native VWF is mediated through domains distal to the ADAMTS-13 spacer, probably thrombospondin-1 repeats. Paper-14158764. It colocalizes with factor VIII ( FVIII) by non-covalent interaction and alters its intracellular trafficking. vWF is also instrumental in maintaining the stability of secreted FVIII. Paper-12489879. 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. When HRECs were exposed to oxygen-glucose deprivation (OGD), clusterin expression increased, whereas von Willebrand factor ( vWF), occludin, and zonula occludens ( ZO-1) markedly decreased. Paper-12492283. ADAMTS-13 prevents inappropriate microvascular platelet aggregation by cleaving VWF between Tyr1605 and Met1606 thereby producing dimers of 176 kd and 140 kd and smaller multimers. Paper-10326505. These markers were: the sulphated epitope MECA-79, the Duffy antigen receptor for chemokines ( DARC), von Willebrand factor, CD31 ( PECAM-1), CD34, CD105 (endoglin) and CD146. Paper-10802874. A statistically significant rise in coagulant factor VIII (FVIII) and von Willebrand factor ( vWF), and slightly rise in u-PA:Ag were observed after G-CSF plus dexamethasone administration. Paper-13077914. A disintegrin and metalloprotease with a thrombospondin type 1 motifs 13 ( ADAMTS-13) regulates hemostasis by cleaving the folded A2 domain of von Willebrand factor ( VWF). Paper-14206676. ADAMTS13 may play a role in arterial thrombosis by cleaving the highly active and thrombogenic ultralarge Von Willebrand Factor ( VWF) multimers into less active VWF multimers. Paper-14115491. Iron induced significant increase in plasma malondialdehyde and IL-8 in monocytes, but had no effect on total antioxidant capacity, CD11b/ CD18 expression, plasma IL-8, vWF and sICAM-1. Paper-15110451. Diabetes is associated with a high incidence of endothelial-binding antibodies which do not correlate with retinopathy, von Willebrand factor, angiotensin-converting enzyme or C-reactive protein. Paper-7175324. In conclusion, there is compelling evidence that GPIbalpha/ VWF interactions and downstream signaling via phospholipase D1 ( PLD1) provide new therapeutic targets in ischemic stroke. Paper-15328969. This TM spike was not correlated with the progressive tissue-type plasminogen activator (t-PA) increase, plasminogen activator inhibitor 1 ( PAI-1), or von Willebrand factor ( vWF) values. Paper-147461. Recent studies revealed that a plasma zinc metalloprotease ADAMTS (a disintegrin and metalloprotease with thrombospondin type 1 motif) 13 cleaves von Willebrand factor in a shear-dependent manner. Paper-10633435. Destabilization of the A1 domain in von Willebrand factor dissociates the A1A2A3 tri-domain and provokes spontaneous binding to glycoprotein Ibalpha and platelet activation under shear stress. Paper-15314098. Intensive multifactorial intervention is associated with reductions in plasma VEGF, vWf, and (in patients without CVD) Ang-2 levels, possibly reflecting an improved vascular profile with treatment. Paper-10939409. The intra-assay coefficients of variation (CV%) for fg and fn bound to vWf were 10.6% and 7.4% (n = 10) respectively, and the inter-assay coefficients of variation were 24.4% and 22.2% (n = 10). Paper-7514404. Effects of C-reactive protein on the release of von Willebrand factor, E-selectin, thrombomodulin and intercellular adhesion molecule-1 from human umbilical vein endothelial cells. Paper-9959012. 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. GrB cleaves VWF with comparable efficiency to ADAMTS-13 and rapidly processes ultra-large VWF multimers released from activated endothelial cells under physiological shear. Paper-12903854. RESULTS: Plasma vWf (P=0.009), IL-6 ( P <0.001), VEGF (P=0.001), and Ang-2 (P=0.001), but not Ang-1 (P=0.635), were higher in diabetic patients with and without CVD than in control subjects. Paper-10939409. CONCLUSIONS: ADAMTS-13 binds to circulating VWF and may therefore be incorporated into a platelet-rich thrombus, where it can immediately cleave VWF that is unfolded by fluid shear stress. Paper-14158764. 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. Blockade of HUVEC ADAMTS-13 activity by antibodies to different ADAMTS-13 domains made it possible to detect the attachment of ADAMTS-13 all along the lengths of HUVEC- secreted VWF strings. Paper-14602459. Two cases also stained positively for epithelial membrane antigen and vimentin, but all of them were negative for von Willebrand factor, CD31, CD34, and binding of Ulex europaeus I lectin. Paper-8074376. 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. Purified thrombopoiesis-stimulating factor (TSF) alone induced a two- to threefold increase, and when used in combination with 10 U/ml IL-3, TSF induced a synergistic five- to sixfold increase in vWF synthesis. Paper-6868195. By coexpression of vWF and various propeptide processing enzymes in COS-1 cells, we here demonstrate that vWF is preferentially processed by the paired dibasic amino acid-cleaving enzyme PACE ( furin). Paper-58808. Expression of the VWF, DTR, CDH5, TIE, and IGFBP7 genes were found to discriminate between cancer patients and "healthy" donors with a receiver operating characteristic curve accuracy of 0.93. Paper-11311969. CONCLUSIONS: Our study suggested that TSP1 played competitively inhibitory role in ADAMTS13 binding and cleaving of VWF, and the potential competition might happen within A2 and A3 domains. Paper-15454502. 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 LPL mass was inversely associated with vWF, suggesting that widespread endothelial cell damage results in a reduction in LPL bound to endothelium in diabetic subjects with microalbuminuria. Paper-1970786. 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. This study used recombinant A1A2A3 tri-domain proteins to demonstrate that A domain association in von Willebrand factor ( VWF) regulates the binding to platelet glycoprotein Ibalpha ( GPIbalpha). Paper-15314098. 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. 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. 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 structure defines a previously unrecognized binding site within GpIbalpha and represents a clear strategy for developing antiplatelet agents targeting the GpIbalpha- VWF interaction allosterically. Paper-14166268. Similarly, patients with AMI had higher levels of IL-6, sVCAM-1, vWF and tissue plasminogen activator (tPA) (p<0.01 vs controls) and lower levels of ATIII (p<0.01 vs controls) and prtC (p<005 vs controls). Paper-12443129. A previously validated image analysis technique was used to assess submucosal vessels for TM and vWF immunoreactivity, and the intestinal wall for total extracellular matrix-associated TGF-beta immunoreactivity. Paper-1164614. A fall in the expression of both these EC antigens was more pronounced in proliferative forms of GN ( PGN) than in non-proliferative GN (NPGN) ( CD31: NPGN vs. PGN, p < 0.02; vWF: NPGN vs. PGN, p < 0.05). Paper-10904525. Addition of hemophilic plasma as a source of vWF did not cause additional improvement, nor did a potent antibody to vWF raised in rabbits inhibit the ability of AHF to shorten the clotting time of vWD plasma. Paper-4535849. We show that deficiency of ADAMTS13 is the molecular mechanism responsible for TTP, and suggest that physiologic proteolysis of VWF and/or other ADAMTS13 substrates is required for normal vascular homeostasis. Paper-9074551. The uFVIII fraction was calculated by dividing the FVIII activity in the supernatant of the FVIII- VWF- complex-free sample by the FVIII activity in the supernatant of the control sample. Paper-10467367. RESULTS: Several PKC inhibitors ( staurosporine, Ro31-8220, myristoylated PKC peptide inhibitor and Go6983) block VEGF- induced but not histamine- induced VWF secretion. Paper-14338671. 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. The cysteine allele of the amino acid polymorphism (AAP) Y/ C1584 in the A2 domain of von Willebrand factor ( VWF) has been shown to correlate with enhanced VWF proteolysis by ADAMTS13. Paper-13109014. 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. Fasting blood glucose levels correlated with vWF antigen, t-PA antigen, and PAI-1 activity, whereas urine albumin excretion correlated with TFPI activity, vWF antigen, and PAI-1 activity. Paper-9259971. 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. 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. RESULTS: Triglycerides, hsCRP, creatinine, IL-6, TNF-alpha, vWF, F1+2, TAT, thrombomodulin, ICAM, VCAM, CD146, PAI-1, leptin, adiponectin and visfatin were elevated in dialyzed patients over controls. Paper-15110453. E-selectin and vWF were not correlated with percent body fat, but were negatively correlated with M ( r= -0.65 and -0.46, both P<0.001) and positively correlated with CRP (r=0.46, and 0.33, both P<0.05). Paper-9396491. The von Willebrand factor pseudogene, previously mapped to chromosome 22, was sublocalized by in situ hybridization using as probe a von Willebrand factor cDNA fragment completely contained in the pseudogenic region. Paper-6224179. 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. Our data suggest that FVIII plays a role in regulating proteolytic processing of VWF by ADAMTS13 under shear stress, which depends on the high-affinity interaction between FVIII and its carrier protein, VWF. Paper-14328179. These results demonstrate that elevated plasma FVIII levels in liver cirrhosis are associated with increased hepatic biosynthesis of VWF and decreased expression of LRP, rather than increased FVIII synthesis. Paper-10435832. The metalloprotease ADAMTS13 efficiently cleaves only the Tyr(1605)-Met(1606) bond in the central A2 domain of multimeric von Willebrand factor ( VWF), even though VWF constitutes only 0.02% of plasma proteins. Paper-12918812. Immunohistochemical analysis showed NF-kappaB protein expression in all the 5 ERMs derived from PDR patients, and that region was partially double-labelled with interleukin-8 ( IL-8) and von Willebrand factor ( vWF). Paper-9923625. To search ADAMTS13 peptide sequences binding to VWF, a lambda-phage library expressing various peptides of ADAMTS13 on the surface was screened using VWF either immobilized or in solution under static condition. Paper-14220794. ADAMTS13 is a highly specific multidomain plasma metalloprotease that regulates the multimeric size and function of von Willebrand factor ( VWF) through cleavage at a single site in the VWF A2 domain. Paper-13810718. 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. Here we show that a mitogen-activated protein kinase ( MAPK), p38, plays an important role in the activation of integrin alphaIIb beta3 induced by VWF and thrombin. Paper-10815678. METHODS AND RESULTS: We measured ADAMTS-13 and VWF antigen levels by ELISAs in stored plasma from a case-control study of 466 MI cases and 484 age- and sex-matched controls from the same north Glasgow population. Paper-14294542. The VWF/ ADAMTS13 ratio was significantly higher in patients with CAF than PAF or controls (2.81 +/- 1.30, 2.34 +/- 0.92, 1.73 +/- 0.83, respectively; P = 0.01 in CAF vs. PAF, P < 0.0001 in CAF vs. controls). Paper-13733851. Our results demonstrate that residues within Y658-Y665 of the ADAMTS13 spacer domain that are targeted by autoantibodies in TTP directly interact with a complementary exosite (E1660-R1668) within the VWF A2 domain. Paper-14180437. Importantly, a single mutation of Tyr(1175) in the C terminus of VEGFR2, a tyrosine residue crucial for embryonic vasculogenesis, abolished vWF release, concomitant with defective activations of both PLCgamma1 and PKA. Paper-13948000. In each of these entities, there is a severe defect in the function of a plasma enzyme, VWF- cleaving metalloprotease ( ADAMTS-13), that normally cleaves hyper-reactive ULVWF multimers into smaller and less adhesive VWF forms. Paper-10326503. Negatively charged binding surfaces on the LRR concave face and anionic region indicate two-step binding kinetics to vWF-A1, which can be regulated by an unmasking mechanism involving conformational change of a key loop. Paper-9170380. In the present study we investigated the effect of adsorbed adhesion proteins (fibrinogen (Fg), fibronectin ( Fn), von Willebrand factor ( vWF) and vitronectin ( Vn)) on the procoagulant activity of adherent platelets. Paper-8511529. 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. Plasma levels of tissue plasminogen activator antigen (t-PA Ag), plasminogen activator inhibitor ( PAI) activity, and factor VIII von Willebrand factor ( vWF) were measured before and 10 minutes after venous occlusion. Paper-7875340. Finally, quantitative real-time RT-PCR analysis performed at 4 and 8 h from cells lining grafts showed that MMP1 mRNA only was increased at 4h whereas vWF, VE-cadherin and KDR were not significantly modified at 4 and 8 h. Paper-13722090. Cultures of MKs from controls performed with or without purified VWF confirmed a positive influence of VWF on platelet production with specific inhibition by an antibody blocking VWF binding to GPIbalpha. Paper-14693002. 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. The minor alleles of rs9399599 and rs1039084 in STXBP5 were associated with lower VWF plasma levels and activity, whereas the minor allele of rs7978987 in STX2 was associated with higher VWF plasma levels and activity. Paper-15561480. 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. The polymorphic systems we have studied are HPA-1 and HPA-3 on the fibrinogen receptor ( GPIIb/IIIa), HPA-2 on the von Willebrand factor receptor (GPIb/IX), and HPA-5 on one of the platelet collagen receptors ( GPIa/IIa). Paper-1108450. The expression of specific endothelial cell markers ( von Willebrand factor, CD31, and the binding and internalization of acetylated low-density lipoprotein) and the smooth muscle cell specific alpha-actin have been evaluated. Paper-13766110. Acquired cases are usually a result of antibodies directed against ADAMTS13 (a disintegrin-like and metalloprotease [reprolysin type] with thrombospondin type 1 motif 13), a protease that cleaves the von Willebrand factor multimers. Paper-10753116. No differences in the allele or genotype frequencies were seen between the study groups for the fibrinogen, prothrombin, factor V, factor VII, vWF, TM, PAI-1, TPO gene, and PLA and HPA-2 genes polymorphisms. Paper-14194188. At optimal zinc and calcium concentrations, ADAMTS13 cleaved VWF with a K(m) (app) of 3.7 +/- 1.4 microg/ml (approximately 15 nM for VWF subunits), which is comparable with the plasma VWF concentration of 5-10 microg/ml. Paper-10826395. Our results indicate that neither FVIII, thrombin-activated FVIII, VWF nor a complex of FVIII and VWF modulate the maturation of human DCs or their capacity to stimulate autologous or allogeneic T cells. Paper-14727679. Antihemophilic factor ( AHF) essentially free of von Willebrand factor ( vWF) was used to determine whether vWF affected the coagulant activity of AHF in a kaolin-activated system using platelet-rich plasma. Paper-4535849. Isolated endothelial cells expressed immunological markers ( vWF, CD105), specific genes ( VE-cadherin, KDR, GATA-2, GATA-3, eNOS), and formed cord-like structures on collagen matrix and in Matrigel assay. Paper-12951867. OBJECTIVES: We investigated the role of PKC and the interactions between PKC and Ca2+ signaling in both VEGF- induced and histamine- induced VWF secretion from human umbilical vein endothelial cells (HUVECs). Paper-14338671. After GPIbalpha binds to the A1 domain of its main ligand VWF, further activation of the platelet via intracellular signalling occurs, allowing other receptors to engage VWF and collagen and thereby reinforcing permanent adhesion. Paper-12995465. Cells variably were immunoreactive for vimentin, CD31, von Willebrand factor VIII, desmin, muscle specific actin, alpha-smooth muscle actin, and skeletal myosin and negative for cytokeratin antigens. Paper-12221809. BACKGROUND: A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 ( ADAMTS-13) may influence von Willebrand factor ( VWF) levels and consequently the risk of myocardial infarction ( MI). Paper-14294542. ADAMTS13 truncated after the first thrombospondin type 1 repeat bound VWF with a K(d) of 206 nm, whereas ADAMTS13 truncated after the spacer domain had a K(d) of 23 nm, which is comparable with that of full-length ADAMTS13. Paper-10742577. 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. RESULTS: As judged by positive staining for endothelial markers vWF and VE-cadherin, the combination of VEGF with fibronectin ( FN) produced significantly more endothelial colonies ( P <.05) than did collagens I or IV or vitronectin. Paper-10369507. The present study indicates that cultivated HOTMEC produce larger quantities of tPA than HUVEC do, possess smaller amounts of von Willebrand factor than HUVEC do, and express thrombomodulin for protein C activation as effectively as HUVEC. Paper-5749301. Antibody 6D1, which blocks platelet GPIb binding of von Willebrand factor, had no effect on thrombin generation, whereas antibody 10E5, which blocks GPIIb/IIIa but not alpha v beta 3 receptors decreased thrombin generation by approximately 25%. Paper-609350. The zinc-protease a disintegrin-like and metalloprotease with thrombospondin type I repeats ( ADAMTS13) cleaves the Tyr(1605)-Met(1606) peptide bond of von Willebrand factor ( VWF), avoiding the accumulation of ultra large VWF multimers. Paper-12910621. 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. Binding was quantitated by ELISA methodologies, based on polyclonal antibodies directed against the proteins studied, in order to express the percentage of moles of fg or fn bound to moles vWf, C[fg/ vWf] or C[fn/ vWf] (mol/mol)%. Paper-7514404. TSP was extremely sensitive to degradation by all enzymes except thrombin, whereas vWF released from the ECM was more resistant to proteolysis than constitutively secreted vWF, and FN was poorly degraded by plasmin. Paper-8352736. At higher collagen coverage densities (0.8 microg/cm2) supporting vWF binding, the inhibition of ERK2 activity by PD 98059 decreased adhesion by 47 +/- 6% at 300 s(-1) and 72 +/- 3% at 1500 s(-1), whereas p38 inhibition had only a small effect. Paper-11135107. Incubation of purified TSP-1 with vWF resulted in formation of thiol-dependent complexes of TSP-1 and vWF, generation of new thiols in vWF, and reduction in the average multimer size of vWF. Paper-8993305. 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 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. 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. In permeable resting cells, punctate staining similar to that reported for fibrinogen (Fbg), thrombospondin ( TSP), fibronectin ( Fn), von Willebrand factor ( VWF), B-thromboglobulin (BTG), and platelet Factor 4 ( PF4) was observed. Paper-5182640. 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. 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. Plasma ADAMTS13 normally cleaves von Willebrand factor within nascent platelet-rich thrombi, and ADAMTS13 deficiency allows unchecked thrombus growth to cause microangiopathic hemolysis, thrombocytopenia, and tissue infarction. Paper-12330324. Obese children displayed significantly elevated values for sICAM-1 (P=0.008), vWF (P=0.034), insulin (P=0.006), homeostasis model assessment for IR (HOMA-IR; P=0.003), C-reactive protein ( CRP) (P<0.001), PAI-1 (P=0.002) and leptin (P<0.001). Paper-12475286. 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. In this study, we examined how IL-4 affects Weibel-Palade bodies (WPBs), EC-specific storage granules capable to store multiple protein components, including von Willebrand factor ( vWF), P-selectin, eotaxin-3, IL-8 and angiopoietin-2 ( Ang-2). Paper-13796297. 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. Recent results with an adhesion blocking antibody (RAM.1) against GPIb beta, which is disulfide linked to GPIb alpha, have suggested a novel function of this subunit in regulating VWF-mediated platelet adhesion, possibly involving its intracellular face. Paper-9701454. The metalloprotease ADAMTS13 is assumed to regulate the functional levels of von Willebrand factor ( VWF) appropriate for normal hemostasis in vivo by reducing VWF multimer size, which directly represents the thrombogenic activity of this factor. Paper-14461375. The platelet fibrinogen (Fg) receptor ( GPIIb/IIIa) is an integrin which plays a critical role in hemostasis by recognizing at least the four adhesive ligands: Fg, fibronectin ( Fn), vitronectin ( Vn), and von Willebrand factor ( vWf). Paper-62463. 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. METHODS: Tissue samples from 40 archival ampullary carcinomas were analysed for COX-2, vascular endothelial growth factor ( VEGF), and an endothelial cell marker von Willebrand factor ( vWF) by immunohistochemistry, using specific antibodies. Paper-11827669. Multivariate logistic regression analysis with adjustment for the same factors revealed that 11 polymorphisms in 11 genes (CAST, CTLA4, F5, GC, GHR, LIPC, PLA2G7, SLC4A1, SLCI8A1, TRH, VWF) showed significant associations with hypertension. Paper-12339895. On another hand, both EL and CG cleave the amino-terminal portion of the GPIb alpha subunit of the GPIb-IX receptor, eliminating the binding site for von Willebrand factor and diminishing the capacity of platelets to interact with this adhesion protein. Paper-11713832. We hypothesized that increased CECs can be related to impaired flow-mediated vasodilatation (FMD, an index of endothelial dysfunction) and elevated plasma von Willebrand factor (vWf, also marking endothelial damage/dysfunction), TF and IL-6 in patients with ACS. Paper-12159559. We demonstrate that irradiation-induced changes in association of NF-Y with HDAC1 and PCAF lead to increased PCAF recruitment to the VWF promoter, increased association of acetylated histone H4 with the VWF promoter and subsequently increased transcription. Paper-12627423. 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. After four months, the cells were re-cultured and phenotyped by flow cytometry and immunohistochemistry, including expression of CD44, CD105, CD90, CD34, CD31, CD141, eNOS and vWF, and compared to their non-cryopreserved counterparts. Paper-12966690. In immunohistochemical analysis, the study group showed significant increases in vWF (P < 0.01), VEGF (P = 0.0012) and CD 31 (P = 0.0023), Wnt3 (P = 0.008) and PCNA (P = 0.0011), and decreases in VCAM (P = 0.0013) and DKK1 (P = 0.0007) than the control group. Paper-14378225. Platelet-type von Willebrand disease (PT- VWD) is a rare autosomal dominant bleeding disorder which is due to a mutation in the gene encoding for platelet glycoprotein Ibalpha ( GPIbalpha) resulting in enhanced affinity for von Willebrand factor ( VWF). Paper-14617805. METHODS: The plasma or serum vWF-cp activity was measured using a sensitive enzyme-linked immunosorbent assay ( ELISA) by detecting the residual collagen binding activity (R-CBA) of von Willebrand factor ( vWF) before and after digestion by vWF-cp. Paper-10453297. These findings may provide novel insight into the structural-function relationship of ADAMTS13 and help us to understand pathogenesis of thrombotic thrombocytopenic purpura and other arterial thromboses associated with compromised VWF proteolysis. Paper-14673461. This shear-induced platelet surface translocation of CD40L, mediated by the von Willebrand factor (VWF)-GP Ibalpha interaction, was enhanced in the presence of a low concentration of epinephrine (100 nM), which by itself, however, could not cause platelet activation. Paper-10688623. PURPOSE: To evaluate the serum levels of von Willebrand factor ( vWF), vascular endothelial growth factor ( VEGF), endothelin-1 ( ET-1), and endothelin-3 ( ET-3) in patients with the isolated, inactive form of Schistosomiasis mansoni. Paper-13534645. Pathologic examination revealed a diffuse proliferation of variably-sized, thin-walled vascular channels lined by flattened endothelium that showed negative immunohistochemical staining for von Willebrand factor, factor VIII-related antigen, CD34 and S-100 protein. Paper-9624269. 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. Tissue sections were obtained by liver biopsy from 25 patients with HBV-associated chronic liver diseases and were examined by immunohistochemistry using anti- CD34, anti- von Willebrand factor ( vWF), and anti-vascular endothelial growth factor ( VEGF) antibodies. Paper-10491532. The amphipathic surfaces in the 228-238 region of the Val 233-containing GPIb alpha protein may associate strongly with complementary surfaces during vWF binding to the GPIb/IX receptor complex and may help explain heightened association of vWF with this receptor in PT-vWD. Paper-43243. Binding of the nuclear protein to the vWF AT-rich sequence in mobility shift assays is inhibited by competition with a consensus Oct-1 binding site and with a silencer octamer-like sequence from the vascular cell adhesion molecule-1 ( VCAM-1) promoter. Paper-1537635. In this report, phylogenetic relationships between Cetacea and artiodactyls are tested with a combination of 15 published data sets plus new DNA sequence data from two nuclear loci, interphotoreceptor retinoid-binding protein ( IRBP) and von Willebrand factor ( vWF). Paper-11602986. These results suggest that shear-dependent VWF- induced platelet activation affects filamin A binding to GpIb-IX-V, and that filamin A binding to the cytoplasmic tail of GpIbalpha regulates proaggregatory tyrosine kinase signaling. Paper-10000356. These were the platelet glycoprotein (GP) receptors GPIIIa, GPIa, GPIbalpha; platelet ligands beta-fibrinogen and von Willebrand Factor ( vWF); interleukins (IL) IL-1RN, and IL-6; adhesion proteins E-selectin and P-selectin; and metalloproteinase MMP-9. Paper-9261030. 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. When CD34+ cells were isolated from midtrimester human fetal lung tissue, then maintained in culture, the isolated cells expressed immunoreactivity for the endothelial cell marker von Willebrand factor and the vascular endothelial growth factor receptors KDR and Flt-1. Paper-9773360. Thus, the observations suggest that the patients with SCD suffer from an acquired ADAMTS-13 deficiency primarily because Hb competitively bound and blocked the proteolysis of VWF, leading to the accumulation of ultra-large VWF multimers in circulation and on endothelium. Paper-13819326. We observed that VEGF stimulation of MAPCs for 14 days results in a significant expression of endothelial-specific gene and/or proteins including von Willebrand factor ( vWF), vascular endothelial-cadherin ( VE-cadherin), VEGF receptor-2 (VEGFR2), and CD31. Paper-12759605. Endothelial cells derived from transplanted bone marrow-derived myeloid lineage progenitors expressed CD31, von Willebrand factor, and Tie2 but did not express the hematopoietic markers CD45 and F4/80 or the pericyte markers desmin and smooth muscle actin. Paper-12205407. Besides glycoprotein Ib (GPIb) and alphaIIbbeta3 integrin, which indirectly interact with collagen via von Willebrand factor ( VWF), several collagen receptors have been identified on platelets, most notably alpha2beta1 integrin and the immunoglobulin (Ig) superfamily member GPVI. Paper-9814507. AIMS: To study long-term effects of enalapril on mass concentrations of tissue plasminogen activator (tPA), plasminogen activator inhibitor ( PAI-1), tPA/ PAI-1- complex and von Willebrand factor ( vWF) in both genders with uncomplicated myocardial infarction. Paper-9383850. 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. 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. 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. In the first of two consecutive studies, relationships between platelet count, von Willebrand factor multimers, ADAMTS-13 activity, plasminogen activator inhibitor-1, and prothrombin time were analyzed in children with and without thrombocytopenia-associated multiple organ failure. Paper-13541015. Elastase induced an almost complete disappearance of intact FN, TSP, and vWF from the ECM at 0.02 units/ml within 5 minutes of incubation at 37 degrees C. Plasmin (0.2 units/ml) was also active on all three substrates, whereas cathepsin G (0.2 units/ml) had a preferential effect on TSP. Paper-8352736. CRP increases during oral contraceptive use were associated with changes in some other acute-phase proteins (fibrinogen, ceruloplasmin, von Willebrand factor [ vWF]) originating from the liver and vessel wall, but not in others ( interleukin-6 [ IL-6], serum amyloid A [ SAA]). Paper-9622565. 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. Using plate binding assay and surface plasmon resonance, we identified a novel ADAMTS13 binding site (K(D) approximately 86 nM) in the region of VWF spanning residues 1874 to 2813, which includes the VWF D4 domain and that interacts with the C-terminal domains of ADAMTS13. Paper-14010442. 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. 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. Thus, the present study investigated the association between plasma von Willebrand factor levels and genetic polymorphisms as follows: ABO blood type, von Willebrand factor -1051G/A (linked with -1793C/G), alpha 2A adrenergic receptor 1780A/G, and alpha 2A adrenergic receptor 2372A/G. Paper-12876710. 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. 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. 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. Endothelial function was assessed by measuring plasma concentrations of the endothelium-derived proteins endothelin (ET), von Willebrand factor ( vWF), and plasminogen activator inhibitor type 1 ( PAI-1) as well as brachial artery flow-mediated, endothelium-dependent vasodilatation ( FMD). Paper-1938532. CONCLUSIONS: These results indicate that genetic polymorphisms in ITGA2 and P2RY1 combine with plasma VWF:Ag levels to modulate baseline platelet reactivity in response to collagen plus EPI, while genetic differences in P2RY1 and GP1BA significantly effect platelet responses to collagen plus ADP. Paper-14150933. The number of these dendritic cells is comparable to that of Langerhans cells in the skin, and dendritic cells show a similar phenotype (CD1a(+) S-100(+) lag(+) CD31(-) CD83(-) CD86(-) and no staining for von Willebrand factor or smooth muscle cell myosin). Paper-8726826. Among subjects with glucose intolerance, levels of PAI-1 and tPA antigen in men and women (P<.01 for trend) and vWF antigen in men (P<.05 for trend) increased significantly across insulin quintiles, but levels of factor VII antigen, fibrinogen, and plasma viscosity did not increase. Paper-2073619. Adiponectin, C-reactive protein ( CRP), interleukin (IL)-6, tumor necrosis factor-alpha, phospholipase A2 (sPLA2), soluble E-selectin (SE-selectin), soluble intracellular adhesion molecule-1, soluble vascular adhesion molecule-1, and von Willebrand factor ( vWF) were measured in baseline samples. Paper-9894158. The strands connecting the platelets are composed of ultralarge multimers of von Willebrand factor (ULVWF) and can be rapidly cleaved when perfused with normal plasma or purified ADAMTS-13 metalloprotease, but not with plasma from patients with either congenital or acquired thrombotic thrombocytopenic purpura (TTP). Paper-10326504. 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. RESULTS: Patients with UA had significantly higher levels of interleukin-6 ( IL-6), soluble vascular cells adhesion molecule (sVCAM-1) and von Willebrand factor ( vWF) (p<0.05 vs controls), and lower levels of antithrombin III ( ATIII) (p<0.01 vs controls) and protein C ( PrtC) (p<0.05 vs controls). Paper-12443129. 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. Conversely, in the presence of a physiological concentration of lyophilized platelets (150 x 10(3)/microl), the half-maximal concentration of FVIII required to accelerate VWF proteolysis by ADAMTS13 reduces by approximately 10-fold (to approximately 0.3 nm) compared with that in the absence of platelets ( approximately 3.0 nm). Paper-15341156. METHODS: Immunohistochemical staining of muscle biopsies (10 DM, 10 SSc, 10 PM, 10 SLE, and 10 non-inflammatory myopathies) with antibodies against von Willebrand factor ( vWF), hypoxia-inducible factor-1beta ( HIF-1beta), beta3 integrin subunit, and vascular endothelial growth factor receptor-1 ( VEGFR-1). Paper-10629700. 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. The aim of this study was to investigate, by immunohistochemistry, the expression of the endothelial marker vWF, of angiogenic bFGF, VEGF and IL-8, of collagenases MMP-2 and MMP-9 and their inhibitors TIMP-1 and TIMP-2, in tissue samples from radiation-induced chronic dermal wounds and healthy control skin. Paper-11638028. Significant positive correlations between M-CSF, and plasma levels of thrombomodulin ( TM), von Willebrand factor antigen ( vWF), thrombin-antithrombin III complex (TAT), prothrombin fragment 1+2 (F1+2), d-dimer products cross-linked fibrin degradation products (d-dimer) and plasmin-antiplasmin complex (PAP) were also found. Paper-11776849. Fab-fragments of the monoclonal antibody 6B4, raised against human glycoprotein Ibalpha ( GPIbalpha), have a powerful antithrombotic effect in baboons by blocking the GPIbalpha binding site for von Willebrand factor ( VWF), without significant prolongation of the skin bleeding time. Paper-14732947. The resulting cell line acquired an almost infinite lifespan, was morphologically unchanged, expressed SV40-antigen, and coexpressed von Willebrand factor ( vWF), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 ( PAI-1), angiotensin conversion enzyme (ACE), and endothelin converting enzyme ( ECE). Paper-738793. By kinetic analysis of recombinant ADAMTS13 constructs, we show that the first thrombospondin-1, Cys-rich, and spacer domains of ADAMTS13 interact with segments of VWF domain A2 between Gln(1624) and Arg(1668), and together these exosite interactions increase the rate of substrate cleavage by at least approximately 300-fold. Paper-12918812. Further studies using the FVIII derivative that lacks an acidic region (a3), an antiplatelet glycoprotein 1balpha IgG, and a purified recombinant VWF-A1 domain or glycoprotein 1balpha-stripped platelets demonstrate that the synergistic rate-enhancing effect of FVIII and platelets depends on their specific binding interactions with VWF. Paper-15341156. Genotyping of angiotensin-converting enzyme, adrenergic receptor beta(3), aldehyde dehydrogenase 2, calpastatin, connexin 37, hepatic lipase, lipoprotein lipase, peroxisome proliferator-activated receptor gamma, thyrotropin-releasing hormone receptor, and von Willebrand factor also was performed in these subjects. Paper-12918536. From our studies, which made use of platelets with GP deficiencies, MAbs, purified vWF, proteolytic fragments of vWF, a synthetic peptide, and in vitro perfusion systems, it appeared that GPIb and GPIIb/IIIa function as receptors for vWF, which binds platelets to connective tissue at sites of vascular lesions (FIGURE 8). Paper-5491618. Plasma markers of platelet activation ( beta-thromboglobulin, BTG) and of endothelium activity (factor VIII/ von Willebrand factor, FVIII/vWf) and plasma renin activity (PRA) were determined in 17 healthy normotensive volunteers and in 21 hypertensives without target-organ damage before and after mental stress (a colour-word conflict test). Paper-5475772. METHODS AND RESULTS: We assessed the -765G>C polymorphism and COX-2 expression in 220 asymptomatic subjects free of cardiovascular disease, in relation to global vascular risk, carotid intima-media thickness (IMT), and inflammatory markers (fibrinogen, C-reactive protein [ CRP], von Willebrand factor [ vWF] and interleukin-6 [ IL-6]). Paper-12022161. Endothelial cells (EC) possess at least two membrane receptors for von Willebrand factor ( vWF), the vitronectin receptor (VNR, alpha(v)beta3), which recognizes an Arg-Gly-Asp (RGD) sequence in the C-terminus of vWF, and glycoprotein Ib alpha ( GP Ib alpha), which interacts with a region in the N-terminal A1 domain of vWF. Paper-1024407. Hemoglobin, hematocrit, thrombelastography, tissue-type plasminogen activator (t-PA), urokinase plasminogen activator ( u-PA), u-PA receptor (u-PAR), plasminogen activator inhibitor-1/2 ( PAI-1/2), D-dimer and von Willebrand factor ( VWF) were determined, and t-PA, u-PA and PAI-1/2 were also determined in endometrial tissue extracts. Paper-12433488. A subset of cultured cells acquired the phenotype of endothelial cells in the presence of vascular endothelial growth factor (e.g., increased expression of KDR and von Willebrand factor positivity), as documented by flow cytometry, immunofluorescence, electron microscopy, and reverse transcription-polymerase chain reaction assays. Paper-13328961. The results show that, at diagnosis, ALL children presented with laboratory signs of increased thrombin generation and fibrin formation (i.e. high TAT and D-dimer levels), fibrinolysis inhibition (i.e. high PAI-1 level), endothelial activation (i.e., high HMW- VWF and soluble P-selectin levels) and inflammation (i.e. high TNF-alpha and IL-6 levels). Paper-15071781. We asked the question whether FVIII itself, FVIII complexed with von Willebrand factor ( VWF) or thrombin- activated FVIII contain danger signals for human DCs that induce the upregulation of costimulatory molecules or the expression of proinflammatory cytokines necessary for effective activation of CD4(+) T cells. Paper-14727679. 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. Of the three cell markers ( CD133, CD34, and the vascular endothelial growth factor receptor 2) that characterize the early functional EPCs, located predominantly in the bone marrow, EPCs obviously lose CD133/ CD34 and start to express CD31, vascular endothelial cadherin, and von Willebrand factor when migrating to the circulation. Paper-9920225. RESEARCH DESIGN AND METHODS: We enrolled 3,094 Japanese type 2 diabetic subjects (62.7% male; aged 61.5 +/- 8.4 years) and determined their genotypes regarding matrix metalloproteinase 9 C-1562T, coagulation factor XII ( F12) C46T, von Willebrand factor ( VWF) G-1051A, and plasminogen activator inhibitor ( PAI-1) 675 4G/5G polymorphisms. Paper-14221238. The following parameters were monitored at the onset of the disease (T0) and after 6 months of follow-up (T1): clinical scores, serum levels of tumor necrosis factor alpha ( TNF-alpha), interleukin 2 ( IL-2), soluble IL-2 receptor (IL-2sRalpha), fibrinogen, von Willebrand factor antigen ( vWf:Ag) and soluble thrombomodulin ( TMD) levels. Paper-12891933. Histamine-induced secretion is dependent on [Ca2+]c but not PKC, whereas VEGF- induced secretion is largely dependent on PKC-delta and significantly less on [Ca2+]c. Our data firmly establish the key role of PKC-delta in VEGF- induced VWF release, but suggest that a third, VEGF-specific, signaling intermediate is required as a PKC-delta coactivator. Paper-14338671. HMGB1, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, von Willebrand Factor ( vWF), angiopoietin-2 ( Ang-2), Prothrombin time (PT), prothrombin fragments 1+2 (PF1+2), soluble thrombomodulin (sTM), protein C ( PC), plasminogen activator inhibitor-1 ( PAI-1), tissue plasminogen activator (tPA) and D-Dimers were measured using standard techniques. Paper-14632341. Analyses of covariance adjusting for age, body mass index, hyperlipidemia, diabetes, smoking, drinking, and antihypertensive medication revealed that 17 polymorphisms in 16 genes ( APOB, CAST, CLCNKB, CTNS, GHR, GYS1, HF1, IKBKAP, KCNJ11, LIPC, LPL, P2RY2, PON2, SLC4A1, TRH, VWF) were significantly associated with blood pressure variations. Paper-12339895. These synonyms are used for gene VWF (von Willebrand factor): vWF, VWD, F8VWF. These accession numbers are used for gene VWF: X04146 (NCBI_GENBANK__AC), Q99806 (UNIPROT__AC), M10321 (NCBI_GENBANK__AC), B4DMS3 (UNIPROT__AC). VWF is a homologue of VWF (von Willebrand factor) from Pan troglodytes. VWF is a homologue of VWF (von Willebrand factor) from Canis lupus familiaris. VWF is a homologue of VWF (von Willebrand factor) from Bos taurus. VWF is a homologue of VWF (von Willebrand factor) from Gallus gallus. VWF is a homologue of Vwf (Von Willebrand factor homolog) from Mus musculus. VWF is a homologue of Vwf (von Willebrand factor) from Rattus norvegicus. VWF is a homologue of vwf (von Willebrand factor) from Danio rerio. Important links ! iHOP - Information Hyperlinked over Proteins . Concept & Implementation by Robert Hoffmann.