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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.nanopub.org/nschema#Nanopublication
http://www.tkuhn.ch/bel2nanopub/RAna95m5n-sCLem7evEKf2OiDZbLb4uWR5SaGuDjJX03E#assertion
http://www.tkuhn.ch/bel2nanopub/RAna95m5n-sCLem7evEKf2OiDZbLb4uWR5SaGuDjJX03E#_1
http://semanticscience.org/resource/SIO_000139
http://www.tkuhn.ch/bel2nanopub/RAna95m5n-sCLem7evEKf2OiDZbLb4uWR5SaGuDjJX03E#_2
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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.informatics.jax.org/marker/MGI:99454
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http://purl.obolibrary.org/obo/BFO_0000066
http://purl.bioontology.org/ontology/MSH/D009132
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http://purl.obolibrary.org/obo/BFO_0000066
http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?id=10090
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http://www.w3.org/2000/01/rdf-schema#label
cat(p(MGI:Irs1)) -> bp(GO:"insulin receptor signaling pathway")
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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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Mice lacking the IRS-1 protein are insulin resistant but do not develop overt diabetes. By contrast, animals lacking IRS-2 exhibit both impaired glucose tolerance and diabetes, which appears to result from a defect in insulin secretion as well as insulin resistance, presumably owing to decreased b-cell proliferation in the pancreas in the face of increased demand for insulin.
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http://www.w3.org/ns/prov#wasQuotedFrom
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Selventa
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http://www.w3.org/ns/prov#hadPrimarySource
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2014-07-03T14:30:01.091+02:00
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