The specific and essential role of MAVS in antiviral innate immune responses.

By Qinmiao Sun, Lijun Sun, Hong-Hsing Liu, Xiang Chen, Rashu B. Seth, J. Forman, Zhijian J. Chen. Immunity, 2006

669 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/a21c5770d5cb76065e20b3930a4cb13b3416a8ca

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Citations in the corpus

Metabolic Pathways In Immune Cell Activation And Quiescence (2013, background): “…defense, a concept further supported by the (metabolically enigmatic) findings that mitochondria are a platform for the induction of type 1 interferon production by retinoic acid-induced gene 1 andmitochondrial antiviral signaling in response to viral infection (Koshiba, 2013; Sun et al., 2006).”
The adaptor protein MITA links virus-sensing receptors to IRF3 transcription factor activation. (2008, background): “Gene-deletion studies indicate that VISA is required for the activation of IRF3 and NF-kB, and VISA-deficient mice exhibit severe deficiency in induction of type I IFNs and proinflammatory cytokines and are susceptible to RNA virus infection (Kumar et al., 2006; Sun et al., 2006).”
RNA recognition and signal transduction by RIG‐I‐like receptors (2009, background): “MDA5-specific stimulation (69, 70), indicating that IPS-1 is indispensable for RLR-mediated signal transduction.”
Plasmacytoid dendritic cells: sensing nucleic acids in viral infection and autoimmune diseases (2008, background): “By contrast, RIG-I-deficient or IPS1-deficient pDCs retain the ability to produce large amounts of IFNα in response to the RNA viruses Newcastle disease virus and Sendai virus, by using the TLR–MyD88 pathwa”
Mitochondria in the regulation of innate and adaptive immunity (2015, positive): “Mice deficient in MAVS are impaired in their ability to produce type I IFNs and thus are highly susceptible to RNA virus infection (Sun et al., 2006).”
Interferons and viruses: an interplay between induction, signalling, antiviral responses and virus countermeasures. (2008, background): “Experiments with knockout mice indicate that this adaptor is essential for responses to both helicases (Kumar et al., 2006; Sun et al., 2006).”
ERIS, an endoplasmic reticulum IFN stimulator, activates innate immune signaling through dimerization (2009, background): “Meanwhile, reports showed that IPS-1/Cardif/MAVS/VISA was not required for dsDNA-caused innate immune activation (12).”
Type I interferons in host defense. (2006, positive): “For example, MAVS-deficient mice infected with VSV suffer severe mortality despite a strong systemic type I IFN response provided by TLR-dependent recognition in pDCs (Sun et al., 2006).”