RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/17486093http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17486093http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17486093http://www.w3.org/2000/01/rdf-schema#comment"Immunoreceptor tyrosine-based activation motifs (ITAMs) are crucial in antigen receptor signaling in acquired immunity. Although receptors associated with the ITAM-bearing adaptors FcRgamma and DAP12 on myeloid cells have been suggested to activate innate immune responses, the mechanism coupling those receptors to 'downstream' signaling events is unclear. The CARMA1-Bcl-10-MALT1 complex is critical for the activation of transcription factor NF-kappaB in lymphocytes but has an unclear function in myeloid cells. Here we report that deletion of the gene encoding the Bcl-10 adaptor-binding partner CARD9 resulted in impaired myeloid cell activation of NF-kappaB signaling by several ITAM-associated receptors. Moreover, CARD9 was required for Toll-like receptor-induced activation of dendritic cells through the activation of mitogen-activated protein kinases. Although Bcl10-/- and Card9-/-mice had similar signaling impairment in myeloid cells, Card11-/-(CARMA1-deficient) myeloid cell responses were normal, and although Card11-/-lymphocytes were defective in antigen receptor-mediated activation, Card9-/-lymphocytes were not. Thus, the activation of lymphoid and myeloid cells through ITAM-associated receptors or Toll-like receptors is regulated by CARMA1-Bcl-10 and CARD9-Bcl-10, respectively."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.org/dc/terms/identifier"doi:10.1038/ni1466"xsd:string
http://purl.uniprot.org/citations/17486093http://purl.org/dc/terms/identifier"doi:10.1038/ni1466"xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Hara H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Hara H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Imanishi T."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Imanishi T."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Koseki H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Koseki H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Morris S.W."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Morris S.W."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Saito T."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Saito T."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Yoshida H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Yoshida H."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Inui M."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Inui M."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Saijo S."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Saijo S."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Takeuchi A."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Takeuchi A."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Ohno N."xsd:string
http://purl.uniprot.org/citations/17486093http://purl.uniprot.org/core/author"Ohno N."xsd:string