Retinoic Acid-inducible Orphan

Retinoic Acid-inducible Gene I (RIG-I) Orphan Receptor

The Retinoic Acid-inducible Gene I (RIG-I) Orphan Receptor, often abbreviated as RIG-I, is a crucial protein in the human body that plays a significant role in the innate immune response to viral infections. This receptor is part of the RIG-I-like receptor (RLR) family, which is involved in detecting viral RNA within cells, thereby initiating an immune response aimed at combating the viral infection.

Function

RIG-I is primarily known for its role in recognizing and binding to specific patterns of RNA, particularly those that are indicative of viral infection. Upon binding to viral RNA, RIG-I undergoes a conformational change that enables it to interact with mitochondrial antiviral-signaling protein (MAVS), also known as IPS-1, VISA, or Cardif. This interaction triggers a signaling cascade that leads to the production of type I interferons and other pro-inflammatory cytokines, which are essential for the antiviral response.

Structure

The structure of RIG-I consists of two N-terminal caspase activation and recruitment domains (CARDs), a central DExD/H-box RNA helicase domain, and a C-terminal domain (CTD). The CARDs are involved in signaling transduction, the helicase domain is responsible for RNA binding and ATP hydrolysis, and the CTD recognizes the 5'-triphosphate end of viral RNA.

Pathway

The RIG-I pathway is initiated when RIG-I binds to viral RNA. This binding facilitates the interaction between the CARDs of RIG-I and MAVS, leading to the activation of transcription factors such as IRF3, IRF7, and NF-κB. These transcription factors then translocate to the nucleus, where they induce the expression of genes involved in the antiviral response, including those encoding type I interferons and pro-inflammatory cytokines.

Clinical Significance

Alterations in the function or expression of RIG-I can have significant implications for viral pathogenesis and the immune response. Overactivation of RIG-I has been associated with autoimmune diseases, where the immune system mistakenly targets the body's own cells. Conversely, viruses have evolved mechanisms to evade RIG-I detection, contributing to viral persistence and pathogenesis.

Research

Research on RIG-I has focused on understanding its role in viral recognition and the subsequent immune response, as well as its potential as a target for antiviral therapies. By modulating RIG-I activity, it may be possible to enhance the immune response to viral infections or mitigate autoimmune responses.

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