ArticleNature immunology2024
UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.
Article in Nature immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Exofacial Epitope-Specific Antibodies Detect GLUT4 Translocation in Adult Human, Rat, and Mouse Skeletal Muscle.Diabetes · 2026Article
- Article
- The RIG-I-like receptor family of immune proteins.Molecular cell · 2025Review
- Interferons in health and disease.Cell · 2025Review
- The immunology of asthma.Nature immunology · 2025Review
- Article
- RNA-Binding Protein Immunoprecipitation 1 (RIP) Assay to Investigate the Interactions Between Viral RNA and Host Proteins.Methods in molecular biology (Clifton, N.J.) · 2025Article
- SCAP/SREBP2-Mediated Cholesterol Biosynthetic Pathway Suppresses Particulate Matter-Induced Macrophage Activation and Airway Inflammation.Journal of inflammation research · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
The cytoplasmic RIG-I-like receptors (RLRs) recognize viral RNA and initiate innate antiviral immunity. RLR signaling also triggers glycolytic reprogramming through glucose transporters (GLUTs), whose role in antiviral immunity is elusive. Here, we unveil that insulin-responsive GLUT4 inhibits RLR signaling independently of glucose uptake in adipose and muscle tissues. At steady state, GLUT4 is trapped at the Golgi matrix by ubiquitin regulatory X domain 9 (UBXN9, TUG). Following RNA virus infection, GLUT4 is released and translocated to the cell surface where it spatially segregates a significant pool of cytosolic RLRs, preventing them from activating IFN-β responses. UBXN9 deletion prompts constitutive GLUT4 translocation, sequestration of RLRs and attenuation of antiviral immunity, whereas GLUT4 deletion heightens RLR signaling. Notably, reduced GLUT4 expression is uniquely associated with human inflammatory myopathies characterized by hyperactive interferon responses. Overall, our results demonstrate a noncanonical UBXN9-GLUT4 axis that controls antiviral immunity via plasma membrane tethering of cytosolic RLRs.
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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 OpenQuestion graph.