| Order number | Description | Quantity | Delivery time | CE |
|---|---|---|---|---|
| TC 16100 | PCI Actibind ELISA Kit | 1 plate | 7 days |
PCI Actibind ELISA KitThe Actibind PCI can be used as a quantitative assay for the determination of active antigen levels of PCI in patients with disseminated intravascular coagulation and in atheriosclerotic disease. Protein C Inhibitor (PCI) is a member of the serine protease inhibitor (Serpin) superfamily with homology to alpha-1-antichymotrypsin, alpha-1-antitrypsin, antithrombin III, ovalbumin and angiotensinogen. PCI with an apparent molecular weight of 57 KD has been described in a variety of biological fluids including blood plasma (4µg/mL), urine (250ng/mL) and seminal plasma (200µg/mL). Glycosaminoglycan (GAG) dependent PCI inhibits activated protein C (APC), twochain urokinase (u-PA), two-chain tissue plasminogen activator (t-PA), thrombin, factor Xa, and factor XIa in reactions stimulated by heparin. However it has recently been shown that the PCI-tissue kallikrein interaction is inhibited by heparin. Glycosaminogylcans may therefore regulate the enzyme specificity of PCI. PCI inhibits its target proteases by forming SDS stable 1:1 complexes. Upon complex formation the reactive site peptide bond of the inhibitor is cleaved by the protease and the carboxy-terminal peptide is released from the inhibitor. Depending on the target protease, complexes dissociate more or less slowly and cleaved inactive PCI (Mr=54,000) and active enzyme are released. Although PCI has been shown to inhibit several enzymes, its precise physiological role has yet to be defined. However, the fact that PCI has been determined in high concentrations in a variety of biological fluids indicates its importance as a physiological serine protease inhibitor whether it be as an inhibitor of a specific serine protease in vivo or as a general inhibitor functioning to protect tissues from protease action. Low values of both Protein C antigen and functional activity of PCI have been determined in patients with disseminated intravascular coagulation and low antigen values in liver disease and high PCI activity in survivors of MI. uPA-PCI complexes are formed in patients undergoing thrombolytic therapy with u-PA when the concentration of u-PA exceeds the inhibitory capacity of plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of u-PA in vivo. |
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