Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus

@article{Meylan2005CardifIA,
  title={Cardif is an adaptor protein in the RIG-I antiviral pathway and is targeted by hepatitis C virus},
  author={Etienne Meylan and Joseph Alphonsus Curran and Kay Hofmann and Darius Moradpour and Marco Binder and Ralf Bartenschlager and Jürg Tschopp},
  journal={Nature},
  year={2005},
  volume={437},
  pages={1167-1172}
}
Antiviral immunity against a pathogen is mounted upon recognition by the host of virally associated structures. One of these viral ‘signatures’, double-stranded (ds) RNA, is a replication product of most viruses within infected cells and is sensed by Toll-like receptor 3 (TLR3) and the recently identified cytosolic RNA helicases RIG-I (retinoic acid inducible gene I, also known as Ddx58) and Mda5 (melanoma differentiation-associated gene 5, also known as Ifih1 or Helicard). Both helicases… 
The antiviral adaptor proteins Cardif and Trif are processed and inactivated by caspases
TLDR
Poliovirus infection triggers a caspase-dependent cleavage of Cardif, suggesting that some viruses may activate caspases not only as a mean to facilitate shedding and replication, but also to impair antiviral responses.
TRADD protein is an essential component of the RIG-like helicase antiviral pathway.
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It is shown that TRADD, a crucial adaptor of tumor necrosis factor receptor (TNFRI), was important in RIG-like helicase (RLH)-mediated signal transduction and is also required for RLH-Cardif-dependent antiviral immune responses.
Hepatitis C Virus Reveals a Novel Early Control in Acute Immune Response
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TLDR
It is revealed that knockdown of NAK-associated protein 1 (NAP1) leads to the down-regulation of IFN-β promoter activation >24 h after poly(I:C) or virus treatment, which is intracellularly initiated by the RIG-I/MDA5 dsRNA-recognition proteins.
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TLDR
The results indicate that Thr-170 phosphorylation and TRIM25-mediated Lys-172 ubiquitination of RIG-I functionally antagonize each other, which keeps Rig-I latent, and enables R IG-I to form a stable complex with MAVS, thereby inducing IFN signal transduction.
N4BP3 Regulates RIG-I-Like Receptor Antiviral Signaling Positively by Targeting Mitochondrial Antiviral Signaling Protein
TLDR
It is suggested that N4BP3 is a critical component of the RIG-I-like receptor (RLR)-mediated innate immune response by targeting MAVS, which also provided insight into the mechanisms of innate antiviral responses.
A RIG-I–like receptor directs antiviral responses to a bunyavirus and is antagonized by virus-induced blockade of TRIM25-mediated ubiquitination
TLDR
It is shown that SFTSV infection induces an antiviral response accompanied by significant induction of antiviral and inflammatory cytokines and that RIG-I plays a main role in this induction by recognizing viral 5′-triphosphorylated RNAs and by signaling via the adaptor mitochondrial antiviral signaling protein.
RNA- and Virus-Independent Inhibition of Antiviral Signaling by RNA Helicase LGP2
TLDR
Results indicate that LGP2 can inhibit antiviral signaling independently of dsRNA or virus infection intermediates by engaging in a protein complex with IPS-1, and provide the first demonstration of protein interaction as an element of negative-feedback regulation of intracellular antiviral signaled by L GP2.
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