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All rights reserved. http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#_6 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#_5 http://www.w3.org/ns/prov#value TAK1, a member of the mitogen-activated kinase kinase kinase family, is activated in vivo by various cytokines, including interleukin-1 (IL-1), or when ectopically expressed together with the TAK1-binding protein TAB1. However, this molecular mechanism of activation is not yet understood. We show here that endogenous TAK1 is constitutively associated with TAB1 and phosphorylated following IL-1 stimulation. Furthermore, TAK1 is constitutively phosphorylated when ectopically overexpressed with TAB1. In both cases, dephosphorylation of TAK1 renders it inactive, but it can be reactivated by preincubation with ATP. A mutant of TAK1 that lacks kinase activity is not phosphorylated either following IL-1 treatment or when coexpressed with TAB1, indicating that TAK1 phosphorylation is due to autophosphorylation. Furthermore, mutation to alanine of a conserved serine residue (Ser-192) in the activation loop between kinase domains VII and VIII abolishes both phosphorylation and activation of TAK1. These results suggest that IL-1 and ectopic expression of TAB1 both activate TAK1 via autophosphorylation of Ser-192. http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#_5 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/10702308 http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#_6 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/10702308 http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#_5 http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk#pubinfo http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk http://purl.org/dc/terms/created 2014-07-03T14:29:50.209+02:00 http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RAD5R6xPILXW43891fcVGnFdSO4RdqZd4SS6gHS5cB-Fk http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234