ELISA/assay

Mouse von Willebrand Factor antigen, vWF:Ag ELISA Kit

MBS723723

48-Strip-Wells

470 USD

ELISA Kit

Mouse von Willebrand Factor antigen, vWF:Ag ELISA Kit

von Willebrand Factor antigen, vWF:Ag

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

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

VWF

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

Q2I0J7_MOUSE

Mouse

This assay has high sensitivity and excellent specificity for detection of vWF. No significant cross-reactivity or interference between vWF and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between vWF 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 ng/mL.

Mouse ELISA Kit

Intended Uses: This vWF ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Mouse vWF. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay VWF ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-vWF antibody and an vWF-HRP conjugate. The assay sample and buffer are incubated together with vWF-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 concentration since vWF from samples and vWF-HRP conjugate compete for the anti-vWF antibody binding site. Since the number of sites is limited, as more sites are occupied by vWF from the sample, fewer sites are left to bind vWF-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The vWF 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: Motility/polarity/chemotaxis; Secreted; Cell adhesion; Extracellular matrix; Secreted, signal peptide. Cellular Component: extracellular matrix; proteinaceous extracellular matrix; endoplasmic reticulum; extracellular region; external side of plasma membrane. Molecular Function: collagen binding; integrin binding; identical protein binding; protein binding; protein homodimerization activity; protease binding; chaperone binding; protein N-terminus binding; immunoglobulin binding; glycoprotein binding. Biological Process: platelet activation; hemostasis; liver development; cell adhesion; blood coagulation; cell-substrate adhesion; protein homooligomerization; placenta development

48-Strip-Wells

470 USD

96-Strip-Wells

675