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http://www.tkuhn.ch/bel2nanopub/RAdFuzPTaHeUmvAaNczIRMGIDNss2bB2yhoWEqjS7UNXQ#_1
http://semanticscience.org/resource/SIO_000139
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0003824
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http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=1338
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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0016301
http://www.tkuhn.ch/bel2nanopub/RAdFuzPTaHeUmvAaNczIRMGIDNss2bB2yhoWEqjS7UNXQ#_4
http://purl.obolibrary.org/obo/RO_0002204
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http://purl.obolibrary.org/obo/BFO_0000066
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http://www.w3.org/2000/01/rdf-schema#label
cat(p(HGNC:C5AR1)) -> kin(p(HGNC:SRC))
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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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1.4
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The response to C5a was blocked by inhibitors of phosphatidylinositol-3-kinase, src kinase, and of the epidermal growth factor (EGF) receptor (EGFR) as well as by neutralizing Abs against the EGFR and heparin-binding EGF-like factor. Furthermore, immune precipitations showed that the EGFR was phosphorylated following stimulation with C5a. The C5aR in endothelial cells thus uses a signaling cascade-transactivation of the EGFR-that does not exist in leukocytes
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Selventa
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2014-07-03T14:30:04.945+02:00
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