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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/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#_5 http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://purl.org/pav/version 1.4 http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#_4 http://www.w3.org/ns/prov#value Nuclear factor-kappaB (NF-kappaB) is a transcription factor critical for key cellular processes, including immune response, apoptosis, and cell cycle progression. A yeast two-hybrid screening, using the Rel homology domain (RHD) of the p65 subunit (RelA) of NF-kappaB as bait, led to the isolation of PIAS3, previously identified as a specific inhibitor of STAT3. We show that PIAS3 can directly associate with p65 using an in vitro pull-down and in vivo coimmunoprecipitation assays. When overexpressed, PIAS3 inhibits NF-kappaB-dependent transcription induced by treatment with tumor necrosis factor alpha (TNF-alpha) or interleukin-1beta or by overexpression of TNF family receptors such as RANK, TNFR1, and CD30 or signal transducers of TNF receptor-associated factors (TRAFs), including TRAF2, TRAF5, and TRAF6. Downregulation of PIAS3 by RNA interference reverses its effect on TNF-alpha-mediated NF-kappaB activation. We found that an N-terminal region of PIAS3 is necessary for both the interaction with p65 and the transcriptional suppression activity. In addition, we found that an LXXLL coregulator signature motif located within the N-terminal region of PIAS3 is the minimal requirement for the interaction with p65. Furthermore, we demonstrate that PIAS3 interferes with p65 binding to the CBP coactivator, thereby resulting in a decreased NF-kappaB-dependent transcription. Taken together, these data suggest that PIAS3 may function in vivo as a modulator in suppressing the transcriptional activity of p65. http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#_4 http://www.w3.org/ns/prov#wasQuotedFrom http://www.ncbi.nlm.nih.gov/pubmed/15140884 http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#_5 http://www.w3.org/2000/01/rdf-schema#label Selventa http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#assertion http://www.w3.org/ns/prov#hadPrimarySource http://www.ncbi.nlm.nih.gov/pubmed/15140884 http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://resource.belframework.org/belframework/1.0/knowledge/large_corpus.bel http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#assertion http://www.w3.org/ns/prov#wasDerivedFrom http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#_4 http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s#pubinfo http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s http://purl.org/dc/terms/created 2014-07-03T14:30:23.380+02:00 http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s http://purl.org/pav/createdBy http://orcid.org/0000-0001-6818-334X http://www.tkuhn.ch/bel2nanopub/RASeyY-Fly8seo1BKlDQi9dBLTIHBhabtU5jntUAiOQ-s http://purl.org/pav/createdBy http://orcid.org/0000-0002-1267-0234