ELISA/assay

Human VWF (Von Willebrand Factor) ELISA Kit

MBS2503678

24-Strip-Wells

215 USD

ELISA Kit

Human VWF (Von Willebrand Factor) ELISA Kit

[VWF]

[VWF; von Willebrand factor; von Willebrand factor; vwf; Von Willebrand factor homolog; von Willebrand antigen II]

[VWF]

[Vwf; Vwf; VWD; F8VWF; AI551257; C630030D09; 6820430P06Rik; B130011O06Rik; vWF]

VWF_MOUSE

Human

2813

This kit recognizes Human VIM in samples. No significant cross-reactivity or interference between Human VIM and analogues was observed.

Store at 4 degree C.

Typical Testing Data/Standard Curve (for reference only)

Samples: Serum, Plasma And Other Biological Fluids. Assay Type: Quantitative Sandwich. Detection Range: 7.81-500pg/mL. Sensitivity: 4.69pg/mL.

Intended Uses: This ELISA kit applies to the in vitro quantitative determination of Human VIM concentrations in serum, plasma and other biological fluids. Principle of the Assay: This ELISA kit uses the Sandwich-ELISA principle. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Human VIM. Standards or samples are added to the micro ELISA plate wells and combined with the specific antibody. Then a biotinylated detection antibody specific for Human VIM and Avidin-Horseradish Peroxidase (HRP) conjugate are added successively to each micro plate well and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Human VIM, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of stop solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of Human VIM. You can calculate the concentration of Human VIM in the samples by comparing the OD of the samples to the standard curve.

86129842

ABC86573.1

Q8CIZ8

44,467 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 Fibrin Clot (Clotting Cascade) Pathway (1110054)

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, signal peptide; Secreted; Motility/polarity/chemotaxis; Extracellular matrix; Cell adhesion. 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; liver development; blood coagulation; protein homooligomerization; cell-substrate adhesion; placenta development

24-Strip-Wells

215 USD

48-Strip-Wells

410

96-Strip-Wells

490

5x96-Strip-Wells

2040

10x96-Strip-Wells

3590