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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RA0RskzzaysemqhI8mAeMU7NcwuaVIPY93RBPwgfyS77U#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=1697
http://www.tkuhn.ch/bel2nanopub/RA0RskzzaysemqhI8mAeMU7NcwuaVIPY93RBPwgfyS77U#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_36080
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http://disease-ontology.org/term/DOID:10283
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http://purl.obolibrary.org/obo/BFO_0000066
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http://purl.obolibrary.org/obo/BFO_0000066
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p(HGNC:CD74) -> bp(GOBP:"cell proliferation")
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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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http://www.w3.org/ns/prov#value
In a recent study by Meyer-Siegler et al. [52] , MIF influenced cell viability and invasiveness. In prostate cancer cells, androgen-independent prostate cancer cells required MIF-activated signal transduction pathways for both growth and invasion, which was in contrast to androgen- dependent cells. They demonstrated that the MIF cell surface receptor CD74 was only detected in androgen- independent tumor cells. Treatments directed against either CD74 or MIF resulted in decreased cell proliferation, MIF secretion and invasion.
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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
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http://purl.org/dc/terms/created
2014-07-03T14:33:25.148+02:00
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