sub:provenance {
  sub:assertion dcterms:description "[Although previous data suggested that symptoms in HAE might be mediated via complement system activation, a combination of recent clinical data, in vitro studies, and analysis of C1INH-deficient mice all indicate that the major mediator of angioedema is bradykinin: (1) a vascular permeability enhancing factor can be generated in vitro in C1INH-depleted, C2-deficient plasma, but not from C1INH-depleted, contact system-deficient plasma; this factor was identified by sequence analysis as bradykinin; (2) bradykinin can be detected in the plasma of HAE patients during attacks of angioedema; (3) in several members of one family, expression of a C1INH variant that inhibits contact system proteases but has defective inhibition of C1r and C1s does not result in HAE; (4) C1INH-deficient (C1INH-/-) mice have a defect in vascular permeability that is suppressed by treatment with specific plasma kallikrein inhibitors and by bradykinin type 2 receptor (Bk2R) antagonists, and is eliminated in C1INH-/-, Bk2R-/- double-deficient mice.]. Sentence from MEDLINE/PubMed, a database of the U.S. National Library of Medicine."@en ;
    wi:evidence dgn-void:source_evidence_literature ;
    sio:SIO_000772 miriam-pubmed:15596403 ;
    prov:wasDerivedFrom dgn-void:BEFREE ;
    prov:wasGeneratedBy eco:ECO_0000203 .
  dgn-void:BEFREE pav:importedOn "2017-02-19"^^xsd:date .
  dgn-void:source_evidence_literature a eco:ECO_0000212 ;
    rdfs:comment "Gene-disease associations inferred from text-mining the literature."@en ;
    rdfs:label "DisGeNET evidence - LITERATURE"@en .
}