ArticleEMBO reports2023
K63-linked polyubiquitination of LGP2 by Riplet regulates RIG-I-dependent innate immune response.
Article in EMBO reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- An ancient anthozoan protein reveals an alternative evolutionary path of antiviral signalling.Nature ecology & evolution · 2026Article
- Lipid nanoparticle-encapsulated microRNA-192: An anti-inflammatory adjuvant that enhances vaccine efficacy in aged mice.Molecular therapy. Nucleic acids · 2026Article
- Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- K63-linked polyubiquitination of LGP2 by Riplet regulates RIG-I-dependent innate immune response.EMBO reports · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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Abstract
Type I interferons (IFNs) exhibit strong antiviral activity and induce the expression of antiviral proteins. Since excessive expression of type I IFNs is harmful to the host, their expression should be turned off at the appropriate time. In this study, we find that post-translational modification of LGP2, a member of the RIG-I-like receptor family, modulates antiviral innate immune responses. The LGP2 protein undergoes K63-linked polyubiquitination in response to cytoplasmic double-stranded RNAs or viral infection. Our mass spectrometry analysis reveals the K residues ubiquitinated by the Riplet ubiquitin ligase. LGP2 ubiquitination occurs with a delay compared to RIG-I ubiquitination. Interestingly, ubiquitination-defective LGP2 mutations increase the expression of type I IFN at a late phase, whereas the mutant proteins attenuate other antiviral proteins, such as SP100, PML, and ANKRD1. Our data indicate that delayed polyubiquitination of LGP2 fine-tunes RIG-I-dependent antiviral innate immune responses at a late phase of viral infection.
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