@prefix dc: .
@prefix this: .
@prefix sub: .
@prefix beldoc: .
@prefix rdfs: .
@prefix rdf: .
@prefix xsd: .
@prefix dce: .
@prefix pav: .
@prefix np: .
@prefix belv: .
@prefix prov: .
@prefix go: .
@prefix Protein: .
@prefix pfh: .
@prefix geneProductOf: .
@prefix hasAgent: .
@prefix hgnc: .
@prefix nch: .
@prefix ProteinComplex: .
@prefix atcc: .
@prefix occursIn: .
@prefix hasAnnotation: .
@prefix species: .
@prefix pubmed: .
@prefix orcid: .
sub:Head {
this: np:hasAssertion sub:assertion;
np:hasProvenance sub:provenance;
np:hasPublicationInfo sub:pubinfo;
a np:Nanopublication .
}
sub:assertion {
nch:Nfkb%20Complex a ProteinComplex: .
sub:_1 hasAgent: sub:_2;
a go:0016301 .
sub:_2 geneProductOf: pfh:CAMK%20Family;
a Protein: .
sub:_3 geneProductOf: hgnc:5992;
a Protein: .
sub:_4 hasAgent: nch:Nfkb%20Complex;
a go:0042789 .
sub:_5 rdf:object sub:_4;
rdf:predicate belv:increases;
rdf:subject sub:_3;
a rdf:Statement .
sub:_6 occursIn: atcc:CRL-1573.aspx, species:9606;
hasAnnotation: sub:_7;
rdf:object sub:_5;
rdf:predicate belv:decreases;
rdf:subject sub:_1;
a rdf:Statement .
sub:_7 dc:subject "TextLocation";
rdf:value "Abstract" .
sub:assertion rdfs:label "kin(p(PFH:\"CAMK Family\")) -| (p(HGNC:IL1B) -> tscript(complex(NCH:\"Nfkb Complex\")))",
"p(HGNC:IL1B) -> tscript(complex(NCH:\"Nfkb Complex\"))" .
}
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:_9;
pav:version "1.6" .
sub:_8 prov:value """However, IL-1β-induced NF-κB activity is attenuated by increased intracellular calcium
in response to ionomycin, UTP, or thapsigargin or by overexpression of CaMKKc
and/or Akt. Ionomycin and CaMKKc overexpression increases Akt phosphorylation
on Thr308 and enzyme activity. Under these conditions or upon overexpression of
wild type Akt, IL-1β-induced IKKβ activity is diminished. Furthermore, a dominant
negative mutant of Akt abolishes IKKβ inhibition by CaMKKc and ionomycin, suggesting
that Akt acts as a mediator of CaMKK signaling to inhibit IL-1β-induced
IKK activity at an upstream target site.""";
prov:wasQuotedFrom pubmed:11976320 .
sub:_9 rdfs:comment "support@belframework.org";
rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:11976320;
prov:wasDerivedFrom beldoc:, sub:_8 .
}
sub:pubinfo {
this: dc:created "2014-07-03T14:29:32.786+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}