@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix rdf: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix belv: . @prefix prov: . @prefix hgnc: . @prefix proteinModification: . @prefix psimod: . @prefix go: . @prefix Protein: . @prefix geneProductOf: . @prefix hasAgent: . @prefix species: . @prefix occursIn: . @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 hgnc:4617; a proteinModification:, psimod:00696 . sub:_2 hasAgent: sub:_3; a go:0016301 . sub:_3 geneProductOf: hgnc:4617; a Protein: . sub:_4 occursIn: species:9606; rdf:object sub:_2; rdf:predicate belv:directlyDecreases; rdf:subject sub:_1; a rdf:Statement . sub:assertion rdfs:label "p(HGNC:GSK3B,pmod(P,S)) =| kin(p(HGNC:GSK3B))" . } 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:_6; pav:version "1.4" . sub:_5 prov:value "Cancer arises from a stepwise accumulation of genetic changes that liberates neoplastic cells from the homeostatic mechanisms that govern normal cell proliferation. In humans, at least four to six mutations are required to reach this state, but fewer seem to be required in mice. By rationalizing the shared and unique elements of human and mouse models of cancer, we should be able to identify the molecular circuits that function differently in humans and mice, and use this knowledge to improve existing models of cancer."; prov:wasQuotedFrom pubmed:12044009 . sub:_6 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:12044009; prov:wasDerivedFrom beldoc:, sub:_5 . } sub:pubinfo { this: dct:created "2014-07-03T14:30:03.502+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }