ELISA/assay

Rat Angiostatin ELISA Kit

MBS725772

48-Strip-Wells

470 USD

ELISA Kit

Rat Angiostatin ELISA Kit

Angiostatin

plasminogen isoform 1; Plasminogen; plasminogen; plasminogen

ANG

PLG; PLG

PLMN_HUMAN

Rat

This assay has high sensitivity and excellent specificity for detection of ANG. No significant cross-reactivity or interference between ANG and analogues was observed. NOTE: Limited by current skills and knowledge, it is impossible for us to complete the cross-reactivity detection between ANG 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 ANG ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Rat ANG. This ELISA kit for research use only, not for therapeutic or diagnostic applications!

Cardiovascular

Principle of the assay: ANG ELISA kit applies the competitive enzyme immunoassay technique utilizing a monoclonal anti-ANG antibody and an ANG-HRP conjugate. The assay sample and buffer are incubated together with ANG-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 ANG concentration since ANG from samples and ANG-HRP conjugate compete for the anti-ANG antibody binding site. Since the number of sites is limited, as more sites are occupied by ANG from the sample, fewer sites are left to bind ANG-HRP conjugate. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The ANG concentration in each sample is interpolated from this standard curve.

4505881

NP_000292.1

NM_000301.3

90,569 Da

Activation Of Matrix Metalloproteinases Pathway (576264); Angiopoietin Receptor Tie2-mediated Signaling Pathway (137917); Blood Clotting Cascade Pathway (198840); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); Degradation Of The Extracellular Matrix Pathway (576263); Dissolution Of Fibrin Clot Pathway (106061); Extracellular Matrix Organization Pathway (576262); Hemostasis Pathway (106028)

The protein encoded by this gene is a secreted blood zymogen that is activated by proteolysis and converted to plasmin and angiostatin. Plasmin dissolves fibrin in blood clots and is an important protease in many other cellular processes while angiostatin inhibits angiogenesis. Defects in this gene are likely a cause of thrombophilia and ligneous conjunctivitis. Two transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Dec 2009]

Plasminogen: Plasmin dissolves the fibrin of blood clots and acts as a proteolytic factor in a variety of other processes including embryonic development, tissue remodeling, tumor invasion, and inflammation. In ovulation, weakens the walls of the Graafian follicle. It activates the urokinase-type plasminogen activator, collagenases and several complement zymogens, such as C1 and C5. Cleavage of fibronectin and laminin leads to cell detachment and apoptosis. Also cleaves fibrin, thrombospondin and von Willebrand factor. Its role in tissue remodeling and tumor invasion may be modulated by CSPG4. Binds to cells. Defects in PLG are the cause of plasminogen deficiency (PLGD). PLGD is characterized by decreased serum plasminogen activity. Two forms of the disorder are distinguished: type 1 deficiency is additionally characterized by decreased plasminogen antigen levels and clinical symptoms, whereas type 2 deficiency, also known as dysplasminogenemia, is characterized by normal, or slightly reduced antigen levels, and absence of clinical manifestations. Plasminogen deficiency type 1 results in markedly impaired extracellular fibrinolysis and chronic mucosal pseudomembranous lesions due to subepithelial fibrin deposition and inflammation. The most common clinical manifestation of type 1 deficiency is ligneous conjunctivitis in which pseudomembranes formation on the palpebral surfaces of the eye progresses to white, yellow-white, or red thick masses with a wood-like consistency that replace the normal mucosa. Belongs to the peptidase S1 family. Plasminogen subfamily. Protein type: Secreted, signal peptide; Protease; Motility/polarity/chemotaxis; EC 3.4.21.7; Secreted. Chromosomal Location of Human Ortholog: 6q26. Cellular Component: extracellular space; cell surface; extrinsic to external side of plasma membrane; plasma membrane; extracellular region. Molecular Function: protein domain specific binding; protein binding; serine-type peptidase activity; serine-type endopeptidase activity; apolipoprotein binding; receptor binding. Biological Process: platelet activation; extracellular matrix organization and biogenesis; tissue remodeling; myoblast differentiation; muscle maintenance; negative regulation of cell proliferation; extracellular matrix disassembly; fibrinolysis; cellular protein metabolic process; platelet degranulation; negative regulation of fibrinolysis; proteolysis involved in cellular protein catabolic process; tissue regeneration; positive regulation of fibrinolysis; blood coagulation; transmembrane transport. Disease: Plasminogen Deficiency, Type I

48-Strip-Wells

470 USD

96-Strip-Wells

675