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http://www.w3.org/1999/02/22-rdf-syntax-ns#type
http://www.nanopub.org/nschema#Nanopublication
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http://www.tkuhn.ch/bel2nanopub/RAQ9YE5DHn_e3-3Fd2pu79Y-rALKVyLl-o1s960vhmzuY#_1
http://purl.obolibrary.org/obo/RO_0002204
http://www.genenames.org/cgi-bin/gene_symbol_report?hgnc_id=5991
http://www.tkuhn.ch/bel2nanopub/RAQ9YE5DHn_e3-3Fd2pu79Y-rALKVyLl-o1s960vhmzuY#_1
http://www.w3.org/1999/02/22-rdf-syntax-ns#type
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http://www.selventa.com/vocabulary/translocationFrom
http://amigo.geneontology.org/amigo/term/GO:0005886
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http://www.selventa.com/vocabulary/translocationTo
http://amigo.geneontology.org/amigo/term/GO:0005737
http://www.tkuhn.ch/bel2nanopub/RAQ9YE5DHn_e3-3Fd2pu79Y-rALKVyLl-o1s960vhmzuY#_3
http://purl.obolibrary.org/obo/RO_0002204
http://www.ncbi.nlm.nih.gov/gene/23118
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p(HGNC:IL1A) -> tloc(p(EGID:23118),GOCCACC:"GO:0005886",GOCCACC:"GO:0005737")
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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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Genetic analysis reveals that IRAK is required for IL-1-induced activation of TAK1. We show that IL-1 stimulation induces the rapid but transient association of IRAK, TRAF6, TAB2, and TAK1. TAB2 is recruited to this complex following translocation from the membrane to the cytosol upon IL-1 stimulation. In IRAK-deficient cells, TAB2 translocation and its association with TRAF6 are abolished. These results suggest that IRAK regulates the redistribution of TAB2 upon IL-1 stimulation and facilitates the formation of a TRAF6-TAB2-TAK1 complex.
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Selventa
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2014-07-03T14:29:54.761+02:00
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