MAVS and MITA are essential adaptor proteins mediating innate antiviral immune
responses against RNA and DNA viruses, respectively. Here we show that RNF115 plays …

Mediator of IRF3 activation (MITA, also named as STING/ERIS/MPYS/TMEM173), is
essential to DNA virus-or cytosolic DNA-triggered innate immune responses. In this study …

Viral infection triggers the formation of mitochondrial antiviral signaling protein (MAVS)
aggregates, which potently promote immune signaling. Autophagy plays an important role in …

In response to virus infection, RIG-I-like receptors (RLRs) sense virus RNA and induce
MAVS to form prion-like aggregates to further propagate antiviral signalling. Although …

Viral infection activates transcription factors NF-κB and IRF3, which collaborate to induce
type I interferons (IFNs) and elicit innate antiviral response. MITA (also known as STING) has …

MAVS is essential for antiviral immunity, but the molecular mechanisms responsible for its
tight regulation remain poorly understood. Here, we show that NLK inhibits the antiviral …

Human innate immunity responds to viral infection by activating the production of interferons
(IFNs) and proinflammatory cytokines. The mitochondrial adaptor molecule MAVS plays a …

The signaling adaptor MAVS forms prion-like aggregates to activate an innate antiviral
immune response after viral infection. However, the molecular mechanisms that regulate …

Activation of MAVS, an adaptor molecule in Rig-I-like receptor (RLR) signaling, is
indispensable for antiviral immunity, yet the molecular mechanisms modulating MAVS …

Highlights•MAVS recruits various downstream molecules through different domains.•Protein
phosphorylation regulates MAVS-mediated signaling.•MAVS aggregation and activation is …