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    <!-- http://purl.obolibrary.org/obo/HP_0012175 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/HP_0012175">
        <rdfs:label>Resistance to activated protein C</rdfs:label>
        <rdfs:subClassOf rdf:resource="http://purl.obolibrary.org/obo/HP_0030780"/>
        <dcterms:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2013-02-23T09:54:07Z</dcterms:date>
        <oboInOwl:hasDbXref>SNOMEDCT_US:421527008</oboInOwl:hasDbXref>
        <ns3:IAO_0000115>Poor anticoagulant response to activated protein C. A plasma is termed &#39;APC resistant&#39; when the addition of exogenous APC fails to prolong its clotting time in an activated partial thromboplastin time assay.</ns3:IAO_0000115>
        <oboInOwl:hasExactSynonym>Activated protein C resistance</oboInOwl:hasExactSynonym>
        <oboInOwl:hasDbXref>UMLS:C0600433</oboInOwl:hasDbXref>
        <rdfs:comment>The protein C pathway is a major anticoagulant mechanism that down-regulates the prothrombin- and intrinsic factor X (FX)-activating complexes via inactivation of their respective cofactors, activated factors V (FVa) and VIII (FVIIIa). Cofactor inactivation occurs by limited proteolysis at certain amino acid positions in FVa and in FVIIIa. These reactions are catalyzed by the serine protease activated protein C (APC) and stimulated by the APC cofactor protein S. Functional defects of the protein C pathway determine a plasma phenotype known as APC resistance, which is a prevalent and important risk factor for venous thrombosis. A plasma is termed &#39;APC resistant&#39; when the addition of exogenous APC fails to prolong its clotting time in an activated partial thromboplastin time (aPTT) assay.</rdfs:comment>
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