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All rights reserved. http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/dc/elements/1.1/title BEL Framework Large Corpus Document http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/authoredBy http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#_5 http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://purl.org/pav/version 20131211 http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#_4 http://www.w3.org/ns/prov#value NF-kappaB-inducing kinase (NIK) has been shown to play an essential role in the NF-kappaB activation cascade elicited by lymphotoxin beta receptor (LTbetaR) signaling. However, the molecular mechanism of this pathway remains unclear. In this report we demonstrate that both NIK and IkappaB kinase alpha (IKKalpha) are involved in LTbetaR signaling and that the phosphorylation of the p65 subunit at serine 536 in its transactivation domain 1 (TA1) plays an essential role. We also found that NF-kappaB could be activated in the LTbetaR pathway without altering the level of the phosphorylation of IkappaB and nuclear localization of p65. By using a heterologous transactivation system in which Gal4-dependent reporter gene is activated by the Gal4 DNA-binding domain in fusion with various portions of p65, we found that TA1 serves as a direct target in the NIK-IKKalpha pathway. In addition, mutation studies have revealed the essential role of Ser-536 within TA1 of p65 in transcriptional control mediated by NIK-IKKalpha. Furthermore, we found that Ser-536 was phosphorylated following the stimulation of LTbetaR, and this phosphorylation was inhibited by the kinase-dead dominant-negative mutant of either NIK or IKKalpha. These observations provide evidence for a crucial role of the NIK-IKKalpha cascade for NF-kappaB activation in LTbetaR signaling. http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#_4 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/12419817 http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#_5 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/12419817 http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/20131211/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#_4 http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E#pubinfo http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E http://purl.org/dc/terms/created 2014-07-03T14:31:56.295+02:00 http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RABuU013jA3XYrzcwikYvbAOsIs8ToOsC1CwoMyiL0h7E http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234