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http://purl.uniprot.org/citations/22749352http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22749352http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22749352http://www.w3.org/2000/01/rdf-schema#comment"The mitochondrial protein MAVS (also known as IPS-1, VISA, and CARDIF) interacts with RIG-I-like receptors (RLRs) to induce type I interferon (IFN-I). NLRX1 is a mitochondrial nucleotide-binding, leucine-rich repeats (NLR)-containing protein that attenuates MAVS-RLR signaling. Using Nlrx1(-/-) cells, we confirmed that NLRX1 attenuated IFN-I production, but additionally promoted autophagy during viral infection. This dual function of NLRX1 paralleled the previously described functions of the autophagy-related proteins Atg5-Atg12, but NLRX1 did not associate with Atg5-Atg12. High-throughput quantitative mass spectrometry and endogenous protein-protein interaction revealed an NLRX1-interacting partner, mitochondrial Tu translation elongation factor (TUFM). TUFM interacted with Atg5-Atg12 and Atg16L1 and has similar functions as NLRX1 by inhibiting RLR-induced IFN-I but promoting autophagy. In the absence of NLRX1, increased IFN-I and decreased autophagy provide an advantage for host defense against vesicular stomatitis virus. This study establishes a link between an NLR protein and the viral-induced autophagic machinery via an intermediary partner, TUFM."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2012.03.025"xsd:string
http://purl.uniprot.org/citations/22749352http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2012.03.025"xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Chen X."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Chen X."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Lei Y."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Lei Y."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Zhang L."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Yu Y."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Yu Y."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Ting J.P."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Ting J.P."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Damania B."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Damania B."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Giguere P.M."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Giguere P.M."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Hiscott J."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Hiscott J."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Moore C.B."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Moore C.B."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Razani B."xsd:string
http://purl.uniprot.org/citations/22749352http://purl.uniprot.org/core/author"Razani B."xsd:string