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http://purl.uniprot.org/citations/25660311http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25660311http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25660311http://www.w3.org/2000/01/rdf-schema#comment"Lipoteichoic acid (LTA) is a component of the cell wall of Gram-positive bacteria and induces a toll-like receptor 2 (TLR2)-mediated inflammatory response upon initial binding to lipopolysaccharide-binding protein (LBP) and subsequent transfer to CD14. In this study, we identified a novel role for the nuclear protein high-mobility group box 1 (HMGB1) in LTA-mediated inflammation. Results of ELISA, surface plasmon resonance and native PAGE electrophoretic mobility shift analyses indicated that HMGB1 binds to LTA in a concentration-dependent manner and that this binding is inhibited by LBP. Native PAGE, fluorescence-based transfer and confocal imaging analyses indicated that HMGB1 catalytically disaggregates LTA and transfers LTA to CD14. NF-κB p65 nuclear transmigration, degradation of IκBα and reporter assay results demonstrated that NF-κB activity in HEK293-hTLR2/6 cells is significantly upregulated by a mixture of LTA and soluble CD14 in the presence of HMGB1. Furthermore, the production of TNF-α and IL-6 in J774A.1 and RAW264.7 cells increased significantly following treatment with a mixture of LTA and HMGB1 compared with treatment with LTA or HMGB1 alone. Thus, we propose that HMGB1 plays an important role in LTA-mediated inflammation by binding to and transferring LTA to CD14, which is subsequently transferred to TLR2 to induce an inflammatory response."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.org/dc/terms/identifier"doi:10.1159/000369972"xsd:string
http://purl.uniprot.org/citations/25660311http://purl.org/dc/terms/identifier"doi:10.1159/000369972"xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Kim Y.H."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Kim Y.H."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lee Y.J."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lee Y.J."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Shin J.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Shin J.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lee H.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lee H.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Choi J.E."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Choi J.E."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lim M."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Lim M."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Kwak M.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Kwak M.S."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Youn J.H."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/author"Youn J.H."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/name"J. Innate Immun."xsd:string
http://purl.uniprot.org/citations/25660311http://purl.uniprot.org/core/name"J. Innate Immun."xsd:string
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