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http://www.tkuhn.ch/bel2nanopub/RAFty0vjtbI58JLg44dweV7bLhC2q7YWAlmtikyMSBuMA#_1
http://purl.obolibrary.org/obo/RO_0002204
http://rgd.mcw.edu/rgdweb/report/gene/main.html?id=2544
http://www.tkuhn.ch/bel2nanopub/RAFty0vjtbI58JLg44dweV7bLhC2q7YWAlmtikyMSBuMA#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.w3.org/1999/02/22-rdf-syntax-ns#object
http://amigo.geneontology.org/amigo/term/GO:0008283
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p(RGD:Egr1) -> bp(GOBP:"cell proliferation")
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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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Approximately 61,000 statements.
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Copyright (c) 2011-2012, Selventa. All rights reserved.
http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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BEL Framework Large Corpus Document
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http://www.w3.org/ns/prov#value
To determine a possible role of Egr-1 in the beta-cell, Egr-1 expression in INS-1 cells was silenced using RNA interference (RNAi). Glucose-stimulated insulin secretion in these cells was then measured using ELISA and cell proliferation was measured by [(3)H]thymidine incorporation. Small interfering RNA (siRNA)-mediated silencing of the Egr-1 gene inhibited its induction by glucose but had no observable effect on glucose-stimulated insulin secretion. However, Egr-1 gene silencing did inhibit proliferation of INS-1 cells in a glucose-independent manner.
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http://www.w3.org/ns/prov#wasQuotedFrom
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http://www.w3.org/2000/01/rdf-schema#label
Selventa
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http://www.tkuhn.ch/bel2nanopub/RAFty0vjtbI58JLg44dweV7bLhC2q7YWAlmtikyMSBuMA
http://purl.org/dc/terms/created
2014-07-03T14:32:48.575+02:00
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