ELISA/assay

Mouse Urokinase plasminogen activator ELISA Kit

MBS721117

48-Strip-Wells-(Comp

470 USD

ELISA Kit

Mouse Urokinase plasminogen activator ELISA Kit

Urokinase plasminogen activator

urokinase plasminogen activator, partial; Urokinase-type plasminogen activator; urokinase-type plasminogen activator; U-plasminogen activator; plasminogen activator, urinary; plasminogen activator, urokinase

UPA

PLAU; PLAU; ATF; QPD; UPA; URK; u-PA; BDPLT5; U-plasminogen activator; uPA

UROK_HUMAN

Mouse

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

Store all reagents at 2-8 degree C.

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

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

Cardiovascular

Principle of the assay: uPA ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for uPA. Standards or samples are then added to the microtiter plate wells and uPA if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of uPA present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for uPA are added to each well to “sandwich” the uPA immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain uPA and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The uPA concentration in each sample is interpolated from this standard curve.

56068043

AAV70488.1

46,908 Da

ATF-2 Transcription Factor Network Pathway (138006); Blood Clotting Cascade Pathway (198840); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); DNA Damage Response (only ATM Dependent) Pathway (198827); Dissolution Of Fibrin Clot Pathway (106061); E2F Transcription Factor Network Pathway (137934); Endochondral Ossification Pathway (198812); FGF Signaling Pathway (137989)

This gene encodes a serine protease involved in degradation of the extracellular matrix and possibly tumor cell migration and proliferation. A specific polymorphism in this gene may be associated with late-onset Alzheimer's disease and also with decreased affinity for fibrin-binding. This protein converts plasminogen to plasmin by specific cleavage of an Arg-Val bond in plasminogen. Plasmin in turn cleaves this protein at a Lys-Ile bond to form a two-chain derivative in which a single disulfide bond connects the amino-terminal A-chain to the catalytically active, carboxy-terminal B-chain. This two-chain derivative is also called HMW-uPA (high molecular weight uPA). HMW-uPA can be further processed into LMW-uPA (low molecular weight uPA) by cleavage of chain A into a short chain A (A1) and an amino-terminal fragment. LMW-uPA is proteolytically active but does not bind to the uPA receptor. Alternatively spliced transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2009]

uPA: Specifically cleave the zymogen plasminogen to form the active enzyme plasmin. Defects in PLAU are the cause of Quebec platelet disorder (QPD). QPD is an autosomal dominant bleeding disorder due to a gain-of-function defect in fibrinolysis. Although affected individuals do not exhibit systemic fibrinolysis, they show delayed onset bleeding after challenge, such as surgery. The hallmark of the disorder is markedly increased PLAU levels within platelets, which causes intraplatelet plasmin generation and secondary degradation of alpha-granule proteins. Belongs to the peptidase S1 family. 2 isoforms of the human protein are produced by alternative splicing. Protein type: EC 3.4.21.73; Motility/polarity/chemotaxis; Secreted, signal peptide; Secreted; Protease. Chromosomal Location of Human Ortholog: 10q22.2. Cellular Component: extracellular space; focal adhesion; cell surface; plasma membrane; extracellular region. Molecular Function: protein binding; serine-type endopeptidase activity. Biological Process: fibrinolysis; regulation of cell adhesion mediated by integrin; regulation of smooth muscle cell migration; smooth muscle cell migration; response to hypoxia; regulation of receptor activity; chemotaxis; blood coagulation; signal transduction; proteolysis; regulation of cell proliferation. Disease: Quebec Platelet Disorder; Alzheimer Disease

48-Strip-Wells-(Competitive)

470 USD

48-Strip-Wells-(Sandwich)

470

96-Strip-Wells-(Competitive)

675

96-Strip-Wells-(Sandwich)

675