{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["7(3)"],"submitter":["Lim S"],"pubmed_abstract":["Transforming growth factor-?1 (TGF-?1) 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-1? must overcome the anti-inflammatory effects of TGF-? to boost pro-inflammatory responses in epithelial cells. Here we show that IL-1? or Lipopolysaccharide (LPS) suppresses TGF-?-induced anti-inflammatory signaling in a NF-?B-independent manner. TRAF6, a key molecule in IL-1? signaling, mediates this suppressive effect through interaction with the type III TGF-? receptor (T?RIII), which is TGF-?-dependent and requires type I TGF-? receptor (T?RI) kinase activity. T?RI phosphorylates T?RIII at residue S829, which promotes the TRAF6/T?RIII interaction and consequent sequestration of T?RIII from the T?RII/T?RI complex. Our data indicate that IL-1? enhances the pro-inflammatory response by suppressing TGF-? signaling through TRAF6-mediated sequestration of T?RIII, which may be an important contributor to the early stages of tumor progression."],"journal":["PloS one"],"pagination":["e32705"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3299683"],"repository":["biostudies-literature"],"pubmed_title":["TRAF6 mediates IL-1?/LPS-induced suppression of TGF-? signaling through its interaction with the type III TGF-? receptor."],"pmcid":["PMC3299683"],"pubmed_authors":["Lim S","Kim B","Bae E","Byun K","Kim HS","Yun C","Kim TA","Letterio J","Lee B","Im JP","Park SH","Kim SJ","Hong S"],"additional_accession":[]},"is_claimable":false,"name":"TRAF6 mediates IL-1?/LPS-induced suppression of TGF-? signaling through its interaction with the type III TGF-? receptor.","description":"Transforming growth factor-?1 (TGF-?1) 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-1? must overcome the anti-inflammatory effects of TGF-? to boost pro-inflammatory responses in epithelial cells. Here we show that IL-1? or Lipopolysaccharide (LPS) suppresses TGF-?-induced anti-inflammatory signaling in a NF-?B-independent manner. TRAF6, a key molecule in IL-1? signaling, mediates this suppressive effect through interaction with the type III TGF-? receptor (T?RIII), which is TGF-?-dependent and requires type I TGF-? receptor (T?RI) kinase activity. T?RI phosphorylates T?RIII at residue S829, which promotes the TRAF6/T?RIII interaction and consequent sequestration of T?RIII from the T?RII/T?RI complex. Our data indicate that IL-1? enhances the pro-inflammatory response by suppressing TGF-? signaling through TRAF6-mediated sequestration of T?RIII, which may be an important contributor to the early stages of tumor progression.","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2021-03-06T08:47:52Z","creation":"2019-03-26T23:12:47Z"},"accession":"S-EPMC3299683","cross_references":{"pubmed":["22427868"],"doi":["10.1371/journal.pone.0032705"]}}