Abstract
RIG-I is a cytosolic receptor recognizing virus-specific RNA
structures and initiates an antiviral signaling that induces the
production of interferons and proinflammatory cytokines.
Because inappropriate RIG-I signaling affects either viral
clearance or immune toxicity, multiple regulations of RIG-I
have been investigated since its discovery as the viral RNA
detector. In this review, we describe the recent progress in
research on the regulation of RIG-I activity or abundance.
Specifically, we focus on the mechanism that modulates RIGI-
dependent antiviral response through post-translational
modifications of or protein-protein interactions with RIG-I.
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