The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Biological activityDetermined by its inhibitory effect against single chain tPA induced cleavage of a chromogenic substrate in Imidazole Buffer at 37oC. Half maximal inhibition against 1.0 µg/ml of single chain tPA was obtained at a concentration of 2.0 µg/ml.
Endotoxin level< 0.100 Eu/µg
% SDS-PAGE. Greater than 95% by SDS-PAGE and HPLC analyses.
Determined by its inhibitory effect against single chain tPA induced cleavage of a chromogenic substrate in Imidazole Buffer at 37oC. Half maximal inhibition against 1.0 µg/ml of single chain tPA was obtained at a concentration of 2.0 µg/ml.
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Preparation and Storage
Stability and Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
ReconstitutionCentrifuge the vial prior to opening. Reconstitute in water to a concentration of 0.1-1.0 mg/ml. This solution can then be diluted into other aqueous buffers and stored at 4oC for 1 week or -20oC for future use.
Endothelial plasminogen activator inhibitor
Plasminogen activator inhibitor 1
Plasminogen activator inhibitor type 1
Serine (or cysteine) proteinase inhibitor
Serine (or cysteine) proteinase inhibitor clade E (nexin plasminogen activator inhibitor type 1) member 1
Serpin peptidase inhibitor clade E
Serpin peptidase inhibitor clade E (nexin plasminogen activator inhibitor type 1) member 1
FunctionThis inhibitor acts as 'bait' for tissue plasminogen activator, urokinase, and protein C. Its rapid interaction with TPA may function as a major control point in the regulation of fibrinolysis.
Tissue specificityFound in plasma and platelets and in endothelial, hepatoma and fibrosarcoma cells.
Involvement in diseaseDefects in SERPINE1 are the cause of plasminogen activator inhibitor-1 deficiency (PAI-1D) [MIM:613329]. It is a hematologic disorder characterized by increased bleeding after trauma, injury, or surgery. Affected females have menorrhagia. The bleeding defect is due to increased fibrinolysis of fibrin blood clots due to deficiency of plasminogen activator inhibitor-1, which inhibits tissue and urinary activators of plasminogen. Note=High concentrations of SERPINE1 seem to contribute to the development of venous but not arterial occlusions.
Sequence similaritiesBelongs to the serpin family.
Post-translational modificationsInactivated by proteolytic attack of the urokinase-type (u-PA) and the tissue-type (TPA), cleaving the 369-Arg- -Met-370 bond.