TRAF6 Mediates IL-1 beta/LPS-Induced Suppression of TGF-beta Signaling through Its Interaction with the Type III TGF-beta Receptor
DC Field | Value | Language |
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dc.contributor.author | Lim, Seunghwan | - |
dc.contributor.author | Bae, Eunjin | - |
dc.contributor.author | Kim, Hae-Suk | - |
dc.contributor.author | Kim, Tae-Aug | - |
dc.contributor.author | Byun, Kyunghee | - |
dc.contributor.author | Kim, Byungchul | - |
dc.contributor.author | Hong, Suntaek | - |
dc.contributor.author | Im, Jong Pil | - |
dc.contributor.author | Yun, Chohee | - |
dc.contributor.author | Lee, Bona | - |
dc.contributor.author | Lee, Bonghee | - |
dc.contributor.author | Park, Seok Hee | - |
dc.contributor.author | Letterio, John | - |
dc.contributor.author | Kim, Seong-Jin | - |
dc.date.available | 2020-02-29T06:44:19Z | - |
dc.date.created | 2020-02-05 | - |
dc.date.issued | 2012-03-12 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16521 | - |
dc.description.abstract | Transforming growth factor-beta 1 (TGF-beta 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 beta must overcome the anti-inflammatory effects of TGF-beta to boost pro-inflammatory responses in epithelial cells. Here we show that IL-1 beta or Lipopolysaccharide (LPS) suppresses TGF-beta-induced anti-inflammatory signaling in a NF-kappa B-independent manner. TRAF6, a key molecule in IL-1 beta signaling, mediates this suppressive effect through interaction with the type III TGF-beta receptor (T beta RIII), which is TGF-beta-dependent and requires type I TGF-beta receptor (T beta RI) kinase activity. T beta RI phosphorylates T beta RIII at residue S829, which promotes the TRAF6/T beta RIII interaction and consequent sequestration of T beta RIII from the T beta RII/T beta RI complex. Our data indicate that IL-1 beta enhances the pro-inflammatory response by suppressing TGF-beta signaling through TRAF6-mediated sequestration of T beta RIII, which may be an important contributor to the early stages of tumor progression. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.subject | GROWTH-FACTOR-BETA | - |
dc.subject | NF-KAPPA-B | - |
dc.subject | TRANSCRIPTIONAL REGULATION | - |
dc.subject | INDEPENDENT ACTIVATION | - |
dc.subject | HEPATOMA-CELLS | - |
dc.subject | CANCER | - |
dc.subject | GENE | - |
dc.subject | DIFFERENTIATION | - |
dc.subject | POLYMORPHISMS | - |
dc.subject | INFLAMMATION | - |
dc.title | TRAF6 Mediates IL-1 beta/LPS-Induced Suppression of TGF-beta Signaling through Its Interaction with the Type III TGF-beta Receptor | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000302381500035 | - |
dc.identifier.doi | 10.1371/journal.pone.0032705 | - |
dc.identifier.bibliographicCitation | PLOS ONE, v.7, no.3 | - |
dc.identifier.scopusid | 2-s2.0-84863271183 | - |
dc.citation.title | PLOS ONE | - |
dc.citation.volume | 7 | - |
dc.citation.number | 3 | - |
dc.contributor.affiliatedAuthor | Bae, Eunjin | - |
dc.contributor.affiliatedAuthor | Byun, Kyunghee | - |
dc.contributor.affiliatedAuthor | Hong, Suntaek | - |
dc.contributor.affiliatedAuthor | Lee, Bonghee | - |
dc.contributor.affiliatedAuthor | Kim, Seong-Jin | - |
dc.type.docType | Article | - |
dc.subject.keywordPlus | GROWTH-FACTOR-BETA | - |
dc.subject.keywordPlus | NF-KAPPA-B | - |
dc.subject.keywordPlus | TRANSCRIPTIONAL REGULATION | - |
dc.subject.keywordPlus | INDEPENDENT ACTIVATION | - |
dc.subject.keywordPlus | HEPATOMA-CELLS | - |
dc.subject.keywordPlus | CANCER | - |
dc.subject.keywordPlus | GENE | - |
dc.subject.keywordPlus | DIFFERENTIATION | - |
dc.subject.keywordPlus | POLYMORPHISMS | - |
dc.subject.keywordPlus | INFLAMMATION | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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