NLRP11 disrupts MAVS signalosome to inhibit type I interferon signaling and virus-induced apoptosis.
EMBO Rep
; 18(12): 2160-2171, 2017 12.
Article
em En
| MEDLINE
| ID: mdl-29097393
ABSTRACT
MAVS signalosome plays an important role in RIG-I-like receptor (RLR)-induced antiviral signaling. Upon the recognition of viral RNAs, RLRs activate MAVS, which further recruits TRAF6 and other signaling proteins to initiate type I interferon (IFN) activation. MAVS signalosome also regulates virus-induced apoptosis to limit viral replication. However, the mechanisms that control the activity of MAVS signalosome are still poorly defined. Here, we report NLRP11, a Nod-like receptor, is induced by type I IFN and translocates to mitochondria to interact with MAVS upon viral infection. Using MAVS as a platform, NLRP11 degrades TRAF6 to attenuate the production of type I IFNs as well as virus-induced apoptosis. Our findings reveal the regulatory role of NLRP11 in antiviral immunity by disrupting MAVS signalosome.
Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Interferon Tipo I
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Apoptose
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Proteínas Adaptadoras de Transdução de Sinal
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Proteínas NLR
Limite:
Humans
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article