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http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=3229
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0016301
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http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080
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http://purl.obolibrary.org/obo/BFO_0000066
http://disease-ontology.org/term/DOID:1107
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http://purl.obolibrary.org/obo/BFO_0000066
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http://resource.belframework.org/belframework/20131211/namespace/selventa-legacy-chemicals/LY%20294002
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a(SCHEM:"LY 294002") -| (p(HGNC:EGF) -> kin(p(HGNC:AKT1)))
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http://www.w3.org/2000/01/rdf-schema#label
p(HGNC:EGF) -> kin(p(HGNC:AKT1))
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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BEL Framework Large Corpus Document
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We employed well established PI3K inhibitors, wortmannin and LY294002, to blunt the PI3K signaling pathway. The phosphorylation of Akt induced by EGF was totally abolished by preincubation with the PI3K inhibitors in TE-2, TE-8, and TE-10 cells (Fig. 6).
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Selventa
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2014-07-03T14:31:36.322+02:00
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