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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RAvbINdBmkkq58iFi6NDrDjnX6Tfz3lexVVcFe7Eyczfo#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=11205
http://www.tkuhn.ch/bel2nanopub/RAvbINdBmkkq58iFi6NDrDjnX6Tfz3lexVVcFe7Eyczfo#_1
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http://purl.obolibrary.org/obo/BFO_0000066
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http://www.selventa.com/vocabulary/increases
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http://www.w3.org/2000/01/rdf-schema#label
p(HGNC:SP1) -> p(HGNC:VEGFA)
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http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
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http://purl.org/dc/elements/1.1/title
BEL Framework Large Corpus Document
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http://purl.org/pav/authoredBy
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1.4
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http://www.w3.org/ns/prov#value
IGF-1 receptor signaling when blocked with anti IGF-1R alpha neutralizing antibody, and when, either the 2.6 kb or the 0.35 kb VPF/VEGF reporter construct was transfected into AsPC-1 cells. The reporter activity of the 2.6 kb VPF/VEGF promoter showed a 50% decrease, and the 0.35kb VPF/VEGF promoter (mainly Sp1 binding sites) showed a 40% decrease compared with that of the IgG control. These results suggested that in AsPC-1 cells, the IGF-1 receptor signaling promotes VPF/VEGF expression mainly through transcriptional regulation, where the transcription factor Sp1 plays an important role.
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http://www.w3.org/ns/prov#wasQuotedFrom
http://www.ncbi.nlm.nih.gov/pubmed/14604996
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
http://www.ncbi.nlm.nih.gov/pubmed/14604996
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2014-07-03T14:30:18.224+02:00
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