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http://purl.uniprot.org/citations/9432981http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9432981http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9432981http://www.w3.org/2000/01/rdf-schema#comment"CD40 activates nuclear factor kappa B (NF kappa B) and the mitogen-activated protein kinase (MAPK) subfamily, including extracellular signal-regulated kinase (ERK). The CD40 cytoplasmic tail interacts with tumor necrosis factor receptor-associated factor (TRAF)2, TRAF3, TRAF5, and TRAF6. These TRAF proteins, with the exception of TRAF3, are required for NF kappa B activation. Here we report that transient expression of TRAF6 stimulated both ERK and NF kappa B activity in the 293 cell line. Coexpression of the dominant-negative H-Ras did not affect TRAF6-mediated ERK activity, suggesting that TRAF6 may activate ERK along a Ras-independent pathway. The deletion mutant of TRAF6 lacking the NH2-terminal domain acted as a dominant-negative mutant to suppress ERK activation by full-length CD40 and suppress prominently ERK activation by a deletion mutant of CD40 only containing the binding site for TRAF6 in the cytoplasmic tail (CD40 delta 246). Transient expression of the dominant-negative H-Ras significantly suppressed ERK activation by full-length CD40, but marginally suppressed ERK activation by CD40 delta 246, compatible with the possibility that TRAF6 is a major transducer of ERK activation by CD40 delta 246, whose activity is mediated by a Ras-independent pathway. These results suggest that CD40 activates ERK by both a Ras-dependent pathway and a Ras-independent pathway in which TRAF6 could be involved."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.org/dc/terms/identifier"doi:10.1084/jem.187.2.237"xsd:string
http://purl.uniprot.org/citations/9432981http://purl.org/dc/terms/identifier"doi:10.1084/jem.187.2.237"xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Inoue J."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Inoue J."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Nakano H."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Nakano H."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Okumura K."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Okumura K."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Yamamoto T."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Yamamoto T."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Okazaki K."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Okazaki K."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Nagaoka H."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Nagaoka H."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Shirakata Y."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Shirakata Y."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Kashiwada M."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Kashiwada M."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Takemori T."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/author"Takemori T."xsd:string
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/date"1998"xsd:gYear
http://purl.uniprot.org/citations/9432981http://purl.uniprot.org/core/date"1998"xsd:gYear