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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.tkuhn.ch/bel2nanopub/RATaUGKffWl2DmUB1hn7Xf_rD-e0nhxXig3H9iKwpeqtk#assertion
http://resource.belframework.org/belframework/20131211/namespace/selventa-named-complexes/Nfkb%20Complex
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://amigo.geneontology.org/amigo/term/GO:0043234
http://www.tkuhn.ch/bel2nanopub/RATaUGKffWl2DmUB1hn7Xf_rD-e0nhxXig3H9iKwpeqtk#_1
http://purl.obolibrary.org/obo/RO_0002204
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http://resource.belframework.org/belframework/20131211/namespace/selventa-named-complexes/Nfkb%20Complex
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http://www.w3.org/2000/01/rdf-schema#label
p(HGNC:RIPK3) -> complex(SCOMP:"Nfkb Complex")
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http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel
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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
Activation of NF-kB induced by overexpression of RIP3 was partially or fully inhibited by the ankyrin and K51R dominant negative mutants of RIP4 kinase domain, suggesting that RIP4 is implicated in the regulation of various NF-kB inducing signaling pathways upstream or at the levels of the IKK activity.
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http://www.w3.org/ns/prov#wasQuotedFrom
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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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2014-07-03T14:31:56.612+02:00
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