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http://purl.uniprot.org/citations/22427868http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22427868http://www.w3.org/2000/01/rdf-schema#comment"Transforming growth factor-β1 (TGF-β1) is an important anti-inflammatory cytokine that modulates and resolves inflammatory responses. Recent studies have demonstrated that inflammation enhances neoplastic risk and potentiates tumor progression. In the evolution of cancer, pro-inflammatory cytokines such as IL-1β must overcome the anti-inflammatory effects of TGF-β to boost pro-inflammatory responses in epithelial cells. Here we show that IL-1β or Lipopolysaccharide (LPS) suppresses TGF-β-induced anti-inflammatory signaling in a NF-κB-independent manner. TRAF6, a key molecule in IL-1β signaling, mediates this suppressive effect through interaction with the type III TGF-β receptor (TβRIII), which is TGF-β-dependent and requires type I TGF-β receptor (TβRI) kinase activity. TβRI phosphorylates TβRIII at residue S829, which promotes the TRAF6/TβRIII interaction and consequent sequestration of TβRIII from the TβRII/TβRI complex. Our data indicate that IL-1β enhances the pro-inflammatory response by suppressing TGF-β signaling through TRAF6-mediated sequestration of TβRIII, which may be an important contributor to the early stages of tumor progression."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0032705"xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Hong S."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Kim H.S."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Kim S.J."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Park S.H."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Lee B."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Kim B."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Lim S."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Bae E."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Yun C."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Kim T.A."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Byun K."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Letterio J."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Im J.P."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/author"Lee B.'"xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/pages"e32705"xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/title"TRAF6 mediates IL-1beta/LPS-induced suppression of TGF-beta signaling through its interaction with the type III TGF-beta receptor."xsd:string
http://purl.uniprot.org/citations/22427868http://purl.uniprot.org/core/volume"7"xsd:string
http://purl.uniprot.org/citations/22427868http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22427868
http://purl.uniprot.org/citations/22427868http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22427868
http://purl.uniprot.org/uniprot/#_Q3TI17-mappedCitation-22427868http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22427868