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The glycoprotein encoded by VWF functions as both an antihemophilic factor carrier and a platelet-vessel wall mediator in the blood coagulation system. 再加上，我们可以发VWF 抗体 (519) 和 VWF 蛋白 (21)和数多这个蛋白质的别的产品。
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Rat (Rattus) VWF ELISA Kit for Sandwich ELISA - ABIN367459
Baraka, Guemei, Gawad: Role of modulation of vascular endothelial growth factor and tumor necrosis factor-alpha in gastric ulcer healing in diabetic rats. in Biochemical pharmacology 2010
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Human VWF ELISA Kit for Sandwich ELISA - ABIN2703573
Ma, Su, Zhang, Ling, Yin, Bai, Ruan: The co-influence of VWD type 2B/2M mutations in the A1 domain and platelet GPIbα on the rate of cleavage to VWF by ADAMTS13. in Thrombosis research 2015
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Rat (Rattus) VWF ELISA Kit for Sandwich ELISA - ABIN416122
Imaoka, Sayama, Suzuki, Jindo, Sanbuissho: Effect of Hypertension on the Occurrence of Micro-hemorrhage in the Pancreatic Islet of Dahl Salt-sensitive Rats. in Journal of toxicologic pathology 2012
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Human VWF ELISA Kit for Sandwich ELISA - ABIN612793
Zimmerman, Ruggeri: von Willebrand disease. in Human pathology 1987
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Human VWF ELISA Kit for Sandwich ELISA - ABIN365425
Tong, Wan, Zhang, Duan, Tang, Chen, Tang, Su: Vascular endothelial cell injury partly induced by mesenteric lymph in heat stroke. in Inflammation 2014
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Human VWF ELISA Kit for Sandwich ELISA - ABIN2685886
Morton, Griffin, Pepper, Barnes: The interaction between collagens and factor VIII/von Willebrand factor: investigation of the structural requirements for interaction. in Thrombosis research 1984
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Rabbit VWF ELISA Kit for Competition ELISA - ABIN415967
Du, Wu, Qing, Wang, Liang, Yu, Tang: Systemic and flap inflammatory response associates with thrombosis in flap venous crisis. in Inflammation 2015
Data suggest that an aspartate at position 1261 is the most critical residue of VWF N-terminal linker for inhibiting binding of VWF A1 domain to GP1BA (显示 GP1BA ELISA试剂盒) on platelets in a model simulating blood flow velocity; network of salt bridges between Asp1261 and rest of VWF A1 domain lock N-terminal linker in place such that binding to GP1BA (显示 GP1BA ELISA试剂盒) is reduced.
In people with dysglycaemia and other cardiovascular risk factors, basal insulin (显示 INS ELISA试剂盒) does not improve the levels of markers of fibrinolysis or von Willebrand factor compared to standard glucose-lowering treatments.
low VWF levels can be associated with significant bleeding and are predominantly due to reductions in VWF synthesis and/or constitutive secretion.
Refrigeration-induced binding of VWF to platelets facilitates their rapid clearance by inducing GPIbalpha (显示 GP1BA ELISA试剂盒)-mediated signaling.
Data show that von Willebrand factor (VWF) is first converted from a compact to linear form by flow, and is subsequently activated to bind platelet glycoprotein Ib alpha polypeptide (显示 ITGAE ELISA试剂盒) (GPIbalpha (显示 GP1BA ELISA试剂盒)) in a tension-dependent manner.
The >30 nm macroglycopeptide separating the two domains of GPIbalpha (显示 GP1BA ELISA试剂盒) transmits force on the VWF-GPIbalpha (显示 GP1BA ELISA试剂盒) bond (whose lifetime is prolonged by leucine-rich repeat domain unfolding) to the juxtamembrane mechanosensitive domain to enhance its unfolding, resulting in unfolding cooperativity at an optimal force.
von Willebrand factor processing and function has been summarized using various biophysical techniques. (Review)
Soluble VWF was statistically elevated in major depressive disorder.
Rare genetic variants in the ADAMTS13 (显示 ADAMTS13 ELISA试剂盒) on Willebrand factor-binding domain contribute to pediatric stroke.
results indicate that VWF multimer accumulation on endothelium, as occurs in congenital thrombotic thrombocytopenic purpura, promotes the activation of the complement alternative pathway that proceeds until C5 cleavage with the formation of C5a and the terminal C5b-9 complex
alterations in glycosylation of vWF and other adhesion proteins associated with the targeting of the alpha1,3-Gal (显示 GAL ELISA试剂盒)-epitope in mutant swine may have salutatory effects on the primate platelet activation observed in these xenografts.
Hemodynamic activation of vWF and increased plasma ADAMTS-13 (显示 ADAMTS13 ELISA试剂盒) may have contributed to reduced high-molecular-weight vWF multimers and impairment of the vWF-platelet aggregation pathway during mechanical circulatory support.
both the gpIb-VWF interaction and the integrin alpha(2 (显示 ITGA2 ELISA试剂盒))beta(1)-collagen interaction contribute to platelet adhesion under high shear stress; integrin alpha(II (显示 GSTA3 ELISA试剂盒))beta(1) makes a greater contribution to adhesion to type I collagen because less VWF is bound
BLOC-2 (显示 HPS6 ELISA试剂盒) subunit HPS6 (显示 HPS6 ELISA试剂盒) deficiency affects the tubulation and secretion of von Willebrand factor from mouse endothelial cells
A novel single-domain antibody against von Willebrand factor A1 domain that interferes with VWF-platelet interactions in vivo. By using this sdAb, show that the A1 domain is pertinent to the participation of VWF in the inflammatory response.
These experiments delineate an unexpected pathway in which microbiota-triggered TLR2 (显示 TLR2 ELISA试剂盒) signaling alters the synthesis of proadhesive VWF by the liver endothelium and favors platelet integrin-dependent thrombus growth.
ADAMTS13 (显示 ADAMTS13 ELISA试剂盒) controls vascular remodeling by modifying VWF reactivity during stroke recovery.
these novel findings support the hypothesis that conformation of the VWF A domains plays a critical role in modulating macrophage-mediated clearance of VWF in vivo.
results revealed localized vascular expression of FVIII (显示 F8 ELISA试剂盒) and von Willebrand factor and identified lymphatic endothelial cell as a major cellular source of FVIII (显示 F8 ELISA试剂盒) in extrahepatic tissues.
Endothelial cell derivedVWF is the major determinant that mediates VWF-dependent ischemic stroke by promoting postischemic thrombo-inflammation.
VWF deficiency reduces the progression of liver fibrosis, suggesting a mechanistic role of elevated plasma VWF levels in cirrhosis
von Willebrand factor exerts beneficial effects in a mouse sepsis model via recruitment of neutrophils to inflammatory sites.
The glycoprotein encoded by this gene functions as both an antihemophilic factor carrier and a platelet-vessel wall mediator in the blood coagulation system. It is crucial to the hemostasis process. Mutations in this gene or deficiencies in this protein result in von Willebrand's disease. An unprocessed pseudogene has been found on chromosome 22.
von Willebrand factor
, coagulation factor VIII VWF