@prefix dcterms: .
@prefix this: .
@prefix sub: .
@prefix beldoc: .
@prefix rdfs: .
@prefix rdf: .
@prefix xsd: .
@prefix dce: .
@prefix pav: .
@prefix np: .
@prefix belv: .
@prefix prov: .
@prefix chebi: .
@prefix entrez: .
@prefix proteinModification: .
@prefix psimod: .
@prefix obo: .
@prefix occursIn: .
@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 {
sub:_1 belv:variantOf entrez:56718;
a proteinModification:, psimod:00696 .
sub:_2 occursIn: obo:CL_0000136, species:10116;
rdf:object sub:_1;
rdf:predicate belv:increases;
rdf:subject chebi:5931;
a rdf:Statement .
sub:assertion rdfs:label "a(CHEBI:\"insulin (human)\") -> p(EGID:56718,pmod(P,S,2448))" .
}
sub:provenance {
beldoc: dce:description "Approximately 61,000 statements.";
dce:rights "Copyright (c) 2011-2012, Selventa. All rights reserved.";
dce:title "BEL Framework Large Corpus Document";
pav:authoredBy sub:_4;
pav:version "20131211" .
sub:_3 prov:value "We show that in freshly isolated rat adipocytes, insulin stimulates the phosphorylation of mTOR on serine 2448, a protein kinase B (PKB) consensus phosphorylation site. This site is also phosphorylated by amino acids, which in contrast to insulin do not activate PKB. Moreover, insulin and amino acids have an additive effect on mTOR phosphorylation, indicating that they act via two independent pathways. Importantly, amino acids, notably leucine, permit insulin to stimulate PKB when PI 3-kinase is inhibited";
prov:wasQuotedFrom pubmed:15479767 .
sub:_4 rdfs:label "Selventa" .
sub:assertion prov:hadPrimarySource pubmed:15479767;
prov:wasDerivedFrom beldoc:, sub:_3 .
}
sub:pubinfo {
this: dcterms:created "2014-07-03T14:32:33.307+02:00"^^xsd:dateTime;
pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 .
}