sub:provenance {
beldoc: dce:description "Approximately 2000 hand curated statements drawn from 57 PubMeds." ;
dce:rights "Copyright (c) 2011-2012, Selventa. All Rights Reserved." ;
dce:title "BEL Framework Small Corpus Document" ;
dc:license "Creative Commons Attribution-Non-Commercial-ShareAlike 3.0 Unported License" ;
pav:authoredBy sub:_6 ;
pav:version "1.6" .
sub:_5 prov:value """In contrast to protein-binding inhibition, evidence has shown that pVHL binds to both
atypical PKC isoforms (l and z) through its b-domain, and in the case of activated
aPKCl, mediates its turnover as part of the E3-ligase function of pVHL [39,40].
Although the functional significance of this inhibition remains elusive,
given the central role for atypical PKCs (especially aPKCz) in establishing cell
polarity in conjunction with PAR6 and the GTPase CDC42 [49], one could envisage
a scenario whereby the loss of pVHL leads to altered cell polarity and, by extension,
aberrant cell migration.""" ;
prov:wasQuotedFrom pubmed:15350900 .
sub:_6 rdfs:comment "support@belframework.org" ;
rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:15350900 ;
prov:wasDerivedFrom beldoc: ,
sub:_5 .
}