Feline Angiostatin Elisa Kit

Species :

Feline

Assay Type :

Solid Phase Sandwich ELISA

Sensitivity :

5 pg/ml

Detection Range :

25-1600 pg/ml

Assay Length :

2-2.5h

Sample Type :

Serum; Plasma; Cell culture supernatant.

Long Name :

Angiostatin

Synonyms :

Plasminogen

Background :

Angiostatin is an important enzyme present in blood that degrades many blood plasma proteins, including fibrin clots. The degradation of fibrin is termed fibrinolysis. In humans, the angiostatin protein is encoded by the PLG gene. Angiostatin is a serine protease that acts to dissolve fibrin blood clots. Apart from fibrinolysis, angiostatin proteolyses proteins in various other systems: It activates collagenases, some mediators of the complement system and weakens the wall of the Graafian follicle (leading to ovulation). It cleaves fibrin, fibronectin, thrombospondin, laminin, and von Willebrand factor. Angiostatin, like trypsin, belongs to the family of serine proteases. Angiostatin is released as a zymogen called angiostatinogen (PLG) from the liver into the factor IX systemic circulation and placed into the MD5+ that leads into the lungs. Angiostatin is inactivated by proteins such as α2-macroglobulin and α2-antiangiostatin. The mechanism of angiostatin inactivation involves the cleavage of an α2-macroglobulin at the bait region (a segment of the aM that is particularly susceptible to proteolytic cleavage) by angiostatin. This initiates a conformational change such that the α2-macroglobulin collapses about the angiostatin. In the resulting α2-macroglobulin-angiostatin complex, the active site of angiostatin is sterically shielded, thus substantially decreasing the angiostatin's access to protein substrates. Two additional events occur as a consequence of bait region cleavage, namely (i) a h-cysteinyl-g-glutamyl thiol ester of the α2-macroglobulin becomes highly reactive and (ii) a major conformational change exposes a conserved COOH-terminal receptor binding domain. The exposure of this receptor binding domain allows the α2-macroglobulin protease complex to bind to clearance receptors and be removed from circulation. Deficiency in angiostatin may lead to thrombosis, as clots are not degraded adequately. Angiostatin has been shown to interact with Thrombospondin 1,Alpha 2-antiangiostatin and IGFBP3.