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http://purl.uniprot.org/citations/18849341http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18849341http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18849341http://www.w3.org/2000/01/rdf-schema#comment"FLN29 was identified as an interferon (IFN)-inducible gene, and it has been shown to suppress Toll-like receptor 4-mediated NF-kappaB activation by binding to TRAF6. To elucidate the physiological roles of FLN29, we generated FLN29-deficient mice. FLN29 deficiency resulted in hyper-response to LPS both in vivo and in vitro, demonstrating the negative regulatory role of FLN29 in TLR4 signaling. Furthermore, we found that FLN29(-/-) mice exhibited increased susceptibility to poly(I:C)-induced septic shock compared with WT mice. FLN29(-/-) fibroblasts were highly resistant to vesicular stomatitis virus infection, and these cells produced more IFN-beta than WT cells did in response to not only intracellular poly(I:C) but also overexpression of IPS-1. Forced expression of FLN29 inhibited the IPS-1-dependent activation of both NF-kappaB and IRF3. We also found that FLN29 could interact with TRIF, IPS-1, TRAF3, and TRAF6. Together, these results suggest that FLN29, in addition to playing a negative regulatory role in the TLR4 signaling pathway, negatively regulates the RIG-I-like helicase signaling pathway at the level of IPS-1/TRAF6 and IPS-1/TRAF3 complexes."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m806923200"xsd:string
http://purl.uniprot.org/citations/18849341http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m806923200"xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Kobayashi T."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Kobayashi T."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Takaesu G."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Takaesu G."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Yoshida R."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Yoshida R."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Yoshimura A."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Yoshimura A."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Sanada T."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Sanada T."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Mashima R."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/author"Mashima R."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/name"J. Biol. Chem."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/name"J. Biol. Chem."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/pages"33858-33864"xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/pages"33858-33864"xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/title"FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathway."xsd:string
http://purl.uniprot.org/citations/18849341http://purl.uniprot.org/core/title"FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathway."xsd:string