sub:provenance {
  sub:assertion dcterms:description "[We present evidence, which indicates that (a) MAK physically associates with AR (MAK and AR are found to be coprecipitated from cell extracts, colocalized in nucleus, and corecruited to prostate-specific antigen promoter in LNCaP as well as in transfected cells); (b) MAK is able to enhance AR transactivation potential in an androgen- and kinase-dependent manner in several prostate cancer cells and synergize with ACTR/steroid receptor coactivator-3 coactivator; (c) small hairpin RNA (shRNA) knocks down MAK expression resulting in the reduction of AR transactivation ability; (d) MAK-shRNA or kinase-dead mutant, when introduced into LNCaP cells, reduces the growth of the cells; and (e) microarray analysis of LNCaP cells carrying kinase-dead MAK mutant showed a significant impediment of AR signaling, indicating that endogenous MAK plays a general role in AR function in prostate cancer cells and likely to be a general coactivator of AR in prostate tissues.]. 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:16951154 ;
    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 .
}