@prefix this: . @prefix sub: . @prefix beldoc: . @prefix rdfs: . @prefix xsd: . @prefix dct: . @prefix dce: . @prefix pav: . @prefix np: . @prefix prov: . @prefix obo: . @prefix Protein: . @prefix hgnc: . @prefix geneProductOf: . @prefix hasPart: . @prefix ProteinComplex: . @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 hasPart: hgnc:3796, sub:_2; occursIn: obo:UBERON_0002367, species:9606; a ProteinComplex: . sub:_2 geneProductOf: hgnc:4659; a Protein: . sub:assertion rdfs:label "complex(p(HGNC:GTF2I),g(HGNC:FOS))" . } 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 "In alpha(2)M*-stimulated cells, moreover, TFII-I bound to the GRP78 promoter as determined by CHIP assay. We also demonstrate binding of TFII-I to the c-fos promoter, consistent with its role in upregulating c-fos gene expression. In non-lymphoid cells, phosphorylated c-Src is an activator of TFII-I. Ligation of GRP78 on 1-LN cells with alpha(2)M* was followed by tyrosine phosphorylation of c-Src as well as TFII-I. We conclude that alpha(2)M*-induced increase in GRP78 synthesis is caused by transcriptional upregulation of TFII-I which binds to the GRP78 promoter and thus potentiates its cell survival and antipoptotic functions in 1-LN prostate cancer cells."; prov:wasQuotedFrom pubmed:19097122 . sub:_4 rdfs:label "Selventa" . sub:assertion prov:hadPrimarySource pubmed:19097122; prov:wasDerivedFrom beldoc:, sub:_3 . } sub:pubinfo { this: dct:created "2014-07-03T14:33:30.884+02:00"^^xsd:dateTime; pav:createdBy orcid:0000-0001-6818-334X, orcid:0000-0002-1267-0234 . }