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    <!-- http://purl.obolibrary.org/obo/HP_0003256 -->

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        <rdfs:label>Abnormality of the coagulation cascade</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/HP_0030780 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/HP_0030780">
        <rdfs:label>Abnormality of the protein C anticoagulant pathway</rdfs:label>
        <rdfs:subClassOf rdf:resource="http://purl.obolibrary.org/obo/HP_0003256"/>
        <dcterms:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2016-03-17T22:14:10Z</dcterms:date>
        <oboInOwl:hasDbXref>UMLS:C4280774</oboInOwl:hasDbXref>
        <ns3:IAO_0000115>An anomaly of the protein C anticoagulant pathway, which serves as a major system for controlling thrombosis, limiting inflammatory responses, and potentially decreasing endothelial cell apoptosis in response to inflammatory cytokines and ischemia. A natural anticoagulant system denoted the protein C pathway exerts its anticoagulant effect by regulating the activity of FVIIIa and FVa. The vitamin K-dependent protein C is the key component of the pathway. Activated protein C (APC) cleaves and inhibits coagulation cofactors FVIIIa and FVa, which result in downregulation of the activity of the coagulation system. The endothelial protein C receptor stimulates the T-TM-mediated activation of protein C on the endothelial cell surface. The two cofactors, protein S and the intact form of FV, enhance the anticoagulant activity of APC.</ns3:IAO_0000115>
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