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http://purl.uniprot.org/citations/18292575http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18292575http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18292575http://www.w3.org/2000/01/rdf-schema#comment"MyD88 and focal adhesion kinase (FAK) are key adaptors involved in signaling downstream of TLR2, TLR4, and integrin alpha5beta1, linking pathogen-associated molecule detection to the initiation of proinflammatory response. The MyD88 and integrin pathways are interlinked, but the mechanism of this cross-talk is not yet understood. In this study we addressed the involvement of Etk, which belongs to the Tec family of tyrosine kinases, in the cross-talk between the integrin/FAK and the MyD88 pathways in fibroblast-like synoviocytes (FLS) and in IL-6 synthesis. Using small interfering RNA blockade, we report that Etk plays a major role in LPS- and protein I/II (a model activator of FAK)-dependent IL-6 release by activated FLS. Etk is associated with MyD88, FAK, and Mal as shown by coimmunoprecipitation. Interestingly, knockdown of Mal appreciably inhibited IL-6 synthesis in response to LPS and protein I/II. Our results also indicate that LPS and protein I/II induced phosphorylation of Etk and Mal in rheumatoid arthritis FLS via a FAK-dependent pathway. In conclusion, our data provide support that, in FLS, Etk and Mal are implicated in the cross-talk between FAK and MyD88 and that their being brought into play is clearly dependent on FAK."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.180.5.3485"xsd:string
http://purl.uniprot.org/citations/18292575http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.180.5.3485"xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Alsaleh G."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Alsaleh G."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Gottenberg J.E."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Gottenberg J.E."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Semaan N."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Semaan N."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Sibilia J."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Sibilia J."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Wachsmann D."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/author"Wachsmann D."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/pages"3485-3491"xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/pages"3485-3491"xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/title"Etk/BMX, a Btk family tyrosine kinase, and Mal contribute to the cross-talk between MyD88 and FAK pathways."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/title"Etk/BMX, a Btk family tyrosine kinase, and Mal contribute to the cross-talk between MyD88 and FAK pathways."xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/volume"180"xsd:string
http://purl.uniprot.org/citations/18292575http://purl.uniprot.org/core/volume"180"xsd:string