Description
Protein S (PS) is a vitamin K-dependent plasma glycoprotein synthesised by hepatocytes, but also by megakaryocytes and other cell types. Its main function is to enhance Activated Protein C (APC)-dependent proteolytic inactivation of factors Va and VIIIa of the coagulation cascade. Thus, regulating thrombin generation, and therefore controlling pro-coagulant activity. In addition, PS works independently from APC by inhibiting both the prothrombinase and tenase complexes. Furthermore, PS is reported to inhibit the activation of thrombin activated fibrinolysis inhibitor, suggesting a potential role in regulating fibrinolysis at the early stages of clot formation. In Circulation, approximately 60% of PS is bound to C4-binding protein, which abolishes its activity whereas 40% is circulating in the free active form. See Also Protein C Antigen Assay (Functional) Plasma, Activated Protein C Resistance (Factor V Leiden) Plasma and Activated Protein C Resistance (Factor V Leiden), RS06Q Mutation, By PCR
Indications
PS deficiency can be either hereditary or acquired and can be either quantitative (types I and III) or qualitative (type II). Thrombotic risk associated with PS deficiency may vary according to the underlying genetic defect. Individuals with heterozygous PS deficiency most commonly present with deep venous thrombosis, pulmonary embolism (PE) and superficial thrombophlebitis. Homozygous and compound heterozygous PS deficiencies are rarely reported and both are usually associated with severe purpura fulminans in the neonatal period. Type I and Type III PS deficiencies both exhibit reduced Free PS levels in plasma. While total PS levels are reduced in Type I deficiency, they are within the normal range in type III.
Sample Type, Quantity & Conditions
2 ml Citrated Plasma Frozen
Special Precautions
Separate & freeze immediately
Normal Range
% Of Pooled Normal Plasma: Male: 67-138 Female: 64-115