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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/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#assertion
http://resource.belframework.org/belframework/1.0/namespace/selventa-named-human-complexes/Nfkb%20Complex
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http://amigo.geneontology.org/amigo/term/GO:0043234
http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_1
http://semanticscience.org/resource/SIO_000139
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http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0042789
http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_2
http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=20389
http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_2
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.ebi.ac.uk/chebi/searchId.do?chebiId=CHEBI_33697
http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_3
http://purl.obolibrary.org/obo/BFO_0000066
http://purl.bioontology.org/ontology/MSH/D017667
http://www.tkuhn.ch/bel2nanopub/RAaq0a5qW12Jt-rZH5j4CXGxygvYiG2p_GPfrHbe6u-V4#_3
http://purl.obolibrary.org/obo/BFO_0000066
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http://www.w3.org/1999/02/22-rdf-syntax-ns#subject
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http://www.w3.org/2000/01/rdf-schema#label
tscript(complex(NCH:"Nfkb Complex")) -> r(HGNC:RETN)
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http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel
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Approximately 61,000 statements.
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http://purl.org/dc/elements/1.1/rights
Copyright (c) 2011-2012, Selventa. All rights reserved.
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http://purl.org/dc/elements/1.1/title
BEL Framework Large Corpus Document
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1.4
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http://www.w3.org/ns/prov#value
Recently, several studies have suggested that metabolic abnormalities are associated with polymorphisms in the human resistin gene [17,18]. Furthermore, several studies, though not all, have reported increased serum resistin levels in patients with obesity, insulin resistance, and/or type 2 diabetes [19,20,21,22,23,24,25,26]. However, the mechanism and importance of increased resistin levels in human metabolic disease are not known. Here we show that the endotoxin lipopolysaccharide (LPS), a potent inflammatory stimulant, dramatically increases resistin production by inducing secretion of inflammatory cytokines such as TNFa. This increase in resistin production is blocked by both aspirin and rosiglitazone, drugs that have dual anti-inflammatory and insulin-sensitizing actions and have been shown to antagonize NF-kB. Indeed, activation of NF-kB is sufficient to induce resistin expression, and loss of NF-kB function abolishes LPS induction of resistin.
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Selventa
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http://www.ncbi.nlm.nih.gov/pubmed/15578112
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2014-07-03T14:30:30.033+02:00
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