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http://www.tkuhn.ch/bel2nanopub/RA2qN-Vkn25r5FqTetyrmXbYsPiKVnvWfwpg-IRl7KQJY#_1
http://semanticscience.org/resource/SIO_000139
http://www.tkuhn.ch/bel2nanopub/RA2qN-Vkn25r5FqTetyrmXbYsPiKVnvWfwpg-IRl7KQJY#_2
http://www.tkuhn.ch/bel2nanopub/RA2qN-Vkn25r5FqTetyrmXbYsPiKVnvWfwpg-IRl7KQJY#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0042789
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http://purl.obolibrary.org/obo/RO_0002204
http://www.informatics.jax.org/marker/MGI:96160
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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://purl.obolibrary.org/obo/BFO_0000066
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tscript(p(MGI:Hmga1)) -> sec(a(SCHEM:"serum insulin"))
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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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Loss of Hmga1 expression, induced in mice by disrupting the Hmga1 gene, considerably decreased insulin receptor expression in the major targets of insulin action, largely impaired insulin signaling and severely reduced insulin secretion, causing a phenotype characteristic of human type 2 diabetes.
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Selventa
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2014-07-03T14:30:35.806+02:00
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