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Retinoic acid-inducible gene I (RIG-I) is a cytosolic pattern recognition receptor (PRR) that plays a central role in the innate immune response to RNA viruses. It detects viral RNA in the cytoplasm and initiates signaling cascades that result in the production of type I interferons and other cytokines essential for antiviral defense. RIG-I discriminates between self-RNA and non-self-RNA primarily by recognizing uncapped or triphosphorylated blunt-ended dsRNA, a signature absent from most host transcripts. Activation of RIG-I triggers interaction with MAVS, leading to TBK1/IKKε activation, IRF3/IRF7 phosphorylation, and induction of IFNα/β gene expression. While best known for its role in antiviral immunity, RIG-I also participates in responses beyond infection, including autoimmune diseases, cancer biology and cardiovascular diseases. It is considered a therapeutic target.
RIG-I agonists bind to RIG-I, activating downstream signaling pathways that lead to the production of type I interferons and other cytokines, ultimately leading to an antiviral state.
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