@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 schem: . @prefix go: . @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 occursIn: obo:UBERON_0004237, species:9606; rdf:object go:0006939; rdf:predicate belv:increases; rdf:subject schem:Calcium; a rdf:Statement . sub:assertion rdfs:label "a(SCHEM:Calcium) -> bp(GOBP:\"smooth muscle contraction\")" . } 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:_3; pav:version "20131211" . sub:_2 prov:value "Recent data implicates ERK (p42/44 kinase) in ANG II-mediated VSMC contraction. Touyz et al. (192) showed that in VSMCs from human peripheral arteries, tyrosine kinases and the ERK signaling cascade play a role in Ca2+ and pHi pathways, which ultimately cause cell contraction; specifically, MEK/ERK may increase Ca2+ availability within cells. "; prov:wasQuotedFrom pubmed:16870827 . sub:_3 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:16870827; prov:wasDerivedFrom beldoc:, sub:_2 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:02.454+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }