ELISA/assay

Rabbit Urokinase plasminogen activator ELISA Kit

MBS723396

48-Strip-Wells

470 USD

ELISA Kit

Rabbit 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

Rabbit

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.

Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Assay Type: Competitive. Sensitivity: 1.0 pg/mL.

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

Cardiovascular

Principle of the assay: uPA ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-uPA antibody and an uPA-HRP conjugate. The assay sample and buffer are incubated together with uPA-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 uPA concentration since uPA from samples and uPA-HRP conjugate compete for the anti-uPA antibody binding site. Since the number of sites is limited, as more sites are occupied by uPA from the sample, fewer sites are left to bind uPA-HRP conjugate. 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: Motility/polarity/chemotaxis; EC 3.4.21.73; Protease; Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: 10q22.2. Cellular Component: extracellular space; focal adhesion; cell surface; extracellular region; plasma membrane. Molecular Function: protein binding; serine-type endopeptidase activity. Biological Process: regulation of cell adhesion mediated by integrin; fibrinolysis; regulation of smooth muscle cell migration; smooth muscle cell migration; response to hypoxia; regulation of receptor activity; signal transduction; chemotaxis; proteolysis; blood coagulation; regulation of cell proliferation. Disease: Quebec Platelet Disorder; Alzheimer Disease

48-Strip-Wells

470 USD

96-Strip-Wells

675