TRADD protein is an essential component of the RIG-like helicase antiviral pathway

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Etat: Public
Version: Final published version
Licence: Non spécifiée
ID Serval
serval:BIB_349C12B082E1
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
TRADD protein is an essential component of the RIG-like helicase antiviral pathway
Périodique
Immunity
Auteur⸱e⸱s
Michallet M. C., Meylan E., Ermolaeva M. A., Vazquez J., Rebsamen M., Curran J., Poeck H., Bscheider M., Hartmann G., Konig M., Kalinke U., Pasparakis M., Tschopp J.
ISSN
1074-7613
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
28
Numéro
5
Pages
651-661
Langue
anglais
Résumé
Upon detection of viral RNA, the helicases RIG-I and/or MDA5 trigger, via their adaptor Cardif (also known as IPS-1, MAVS, or VISA), the activation of the transcription factors NF-kappaB and IRF3, which collaborate to induce an antiviral type I interferon (IFN) response. FADD and RIP1, known as mediators of death-receptor signaling, are implicated in this antiviral pathway; however, the link between death-receptor and antiviral signaling is not known. Here we showed that TRADD, a crucial adaptor of tumor necrosis factor receptor (TNFRI), was important in RIG-like helicase (RLH)-mediated signal transduction. TRADD is recruited to Cardif and orchestrated complex formation with the E3 ubiquitin ligase TRAF3 and TANK and with FADD and RIP1, leading to the activation of IRF3 and NF-kappaB. Loss of TRADD prevented Cardif-dependent activation of IFN-beta, reduced the production of IFN-beta in response to RNA viruses, and enhanced vesicular stomatitis virus replication. Thus, TRADD is not only an essential component of proinflammatory TNFRI signaling, but is also required for RLH-Cardif-dependent antiviral immune responses
Mots-clé
Adaptor Proteins,Signal Transducing, Animals, Biochemistry, Dna, DNA Helicases, Fas-Associated Death Domain Protein, GTPase-Activating Proteins, Humans, immunology, Interferon Regulatory Factor-3, Interferon Type I, Membrane Proteins, metabolism, Mice, Mice,Mutant Strains, Mice,Knockout, Necrosis, Nerve Tissue Proteins, NF-kappa B, physiology, Proteins, Rhabdoviridae Infections, Rna, Signal Transduction, Switzerland, TNF Receptor-Associated Death Domain Protein, TNF Receptor-Associated Factor 3, Transcription Factors, Ubiquitin, Ubiquitin-Protein Ligases, Vesiculovirus, virology
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/01/2009 22:14
Dernière modification de la notice
06/04/2023 5:53
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