ELISA/assay

Human von Willebrand Factor antigen, vWF:Ag ELISA Kit

MBS733078

48-Strip-Wells

470 USD

ELISA Kit

Human von Willebrand Factor antigen, vWF:Ag ELISA Kit

von Willebrand Factor antigen, vWF:Ag

Human von Willebrand Factor antigen, vWF:Ag ELISA Kit; von Willebrand Factor antigen, vWF:Ag; von Willebrand Factor antigen, vWF:Ag ELISA Kit (Human)

VWF; VWF; von Willebrand factor; OTTMUSP00000025031; Von Willebrand factor homolog

VWF

Vwf; Vwf; VWD; F8VWF; AI551257; C630030D09; 6820430P06Rik; B130011O06Rik

Q2I0J7_MOUSE

Human

This assay has high sensitivity and excellent specificity for detection of vWF Ag. No significant cross-reactivity or interference between vWF Ag and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between vWF Ag and all the analogues, therefore, cross reaction may still exist in some cases.

Store all reagents at 2-8 degree C

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 0.1 u/mL.

Intended Uses: This vWF Ag ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human vWF Ag. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Human ELISA Kit

Principle of the Assay: vWF Ag ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-vWF Ag antibody and an vWF Ag-HRP conjugate. The assay sample and buffer are incubated together with vWF Ag-HRP conjugate in pre-coated plate for one hour. After the incubation period, the wells are decanted and washed five times. The wells are then incubated with a substrate for HRP enzyme. The product of the enzyme-substrate reaction forms a blue colored complex. Finally, a stop solution is added to stop the reaction, which will then turn the solution yellow. The intensity of color is measured spectrophotometrically at 450nm in a microplate reader. The intensity of the color is inversely proportional to the vWF Ag concentration since vWF Ag from samples and vWF Ag-HRP conjugate compete for the anti-vWF Ag antibody binding site. Since the number of sites is limited, as more sites are occupied by vWF Ag from the sample, fewer sites are left to bind vWF Ag-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The vWF Ag concentration in each sample is interpolated from this standard curve.

86129842

Q2I0J7

309,102 Da

Blood Clotting Cascade Pathway (198388); Complement And Coagulation Cascades Pathway (198335); Complement And Coagulation Cascades Pathway (83270); Complement And Coagulation Cascades Pathway (484); ECM-receptor Interaction Pathway (83265); ECM-receptor Interaction Pathway (479); Focal Adhesion Pathway (198353); Focal Adhesion Pathway (83264); Focal Adhesion Pathway (478); Formation Of Platelet Plug Pathway (366293)

VWF: Important in the maintenance of hemostasis, it promotes adhesion of platelets to the sites of vascular injury by forming a molecular bridge between sub-endothelial collagen matrix and platelet-surface receptor complex GPIb-IX-V. Also acts as a chaperone for coagulation factor VIII, delivering it to the site of injury, stabilizing its heterodimeric structure and protecting it from premature clearance from plasma. Defects in VWF are the cause of von Willebrand disease type 1 (VWD1). A common hemorrhagic disorder due to defects in von Willebrand factor protein and resulting in impaired platelet aggregation. Von Willebrand disease type 1 is characterized by partial quantitative deficiency of circulating von Willebrand factor, that is otherwise structurally and functionally normal. Clinical manifestations are mucocutaneous bleeding, such as epistaxis and menorrhagia, and prolonged bleeding after surgery or trauma. Defects in VWF are the cause of von Willebrand disease type 2 (VWD2). A hemorrhagic disorder due to defects in von Willebrand factor protein and resulting in impaired platelet aggregation. Von Willebrand disease type 2 is characterized by qualitative deficiency and functional anomalies of von Willebrand factor. It is divided in different subtypes including 2A, 2B, 2M and 2N (Normandy variant). The mutant VWF protein in types 2A, 2B and 2M are defective in their platelet- dependent function, whereas the mutant protein in type 2N is defective in its ability to bind factor VIII. Clinical manifestations are mucocutaneous bleeding, such as epistaxis and menorrhagia, and prolonged bleeding after surgery or trauma. Defects in VWF are the cause of von Willebrand disease type 3 (VWD3). A severe hemorrhagic disorder due to a total or near total absence of von Willebrand factor in the plasma and cellular compartments, also leading to a profound deficiency of plasmatic factor VIII. Bleeding usually starts in infancy and can include epistaxis, recurrent mucocutaneous bleeding, excessive bleeding after minor trauma, and hemarthroses. Protein type: Secreted; Cell adhesion; Motility/polarity/chemotaxis; Secreted, signal peptide; Extracellular matrix. Cellular Component: extracellular matrix; proteinaceous extracellular matrix; endoplasmic reticulum; extracellular region; external side of plasma membrane. Molecular Function: integrin binding; collagen binding; identical protein binding; protein binding; protein homodimerization activity; protease binding; chaperone binding; immunoglobulin binding; protein N-terminus binding; glycoprotein binding. Biological Process: platelet activation; hemostasis; cell adhesion; blood coagulation; liver development; protein homooligomerization; cell-substrate adhesion; placenta development

48-Strip-Wells

470 USD

96-Strip-Wells

675