ArticleScience advances2024
Endosomes serve as signaling platforms for RIG-I ubiquitination and activation.
Article in Science advances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Structural characterization of the human CC2D1A fragment associated with non-syndromic intellectual disability (NSID).Bioscience reports · 2026Article
- Integrative proteomics and lipidomics reveals dual roles for lipid droplets in the host cell antiviral response.Nature communications · 2026Article
- SPRY domains encode ubiquitin ligase specificity for ZAP and RIG-I.PLoS pathogens · 2026Article
- Endothelial JAML inhibits inflammation and atherosclerosis through TRIM25-mediated STAT1 ubiquitination.Cellular & molecular biology letters · 2026Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).International journal of molecular medicine · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RIG-I-like receptors (RLRs) are cytosolic RNA sensors critical for antiviral immunity. RLR activation is regulated by polyubiquitination and oligomerization following RNA binding. Yet, little is known about how RLRs exploit subcellular organelles to facilitate their posttranslational modifications and activation. Endosomal adaptor TAPE regulates the endosomal TLR and cytosolic RLR pathways. The potential interplay between RIG-I signaling and endosomes has been explored. Here, we report that endosomes act as platforms for facilitating RIG-I polyubiquitination and complex formation. RIG-I was translocated onto endosomes to form signaling complexes upon activation. Ablation of endosomes impaired RIG-I signaling to type I IFN activation. TAPE mediates the interaction and polyubiquitination of RIG-I and TRIM25. TAPE-deficient myeloid cells were defective in type I IFN activation upon RNA ligand and virus challenges. Myeloid TAPE deficiency increased the susceptibility to RNA virus infection in vivo. Our work reveals endosomes as signaling platforms for RIG-I activation and antiviral immunity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.