ArticleiScience2020
Upstream ORFs Prevent MAVS Spontaneous Aggregation and Regulate Innate Immune Homeostasis.
Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Elevated CHAF1A Suppresses Type I Interferon Production and Causes Immunotherapy Resistance in Esophageal Squamous Cell Carcinoma.Cancer immunology research · 2026Article
- Review
- Inflammatory mitochondrial signalling and viral mimicry in cancer.Journal of translational medicine · 2025Review
- Induction of the ISR by AB5 subtilase cytotoxin drives type-I IFN expression in pDCs via STING activation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- E3 Ubiquitin Ligases: The Operators of the Ubiquitin Code That Regulates the RLR and cGAS-STING Pathways.International journal of molecular sciences · 2022Review
- Review
- Crosstalk between mitophagy and innate immunity in viral infection.Frontiers in microbiology · 2022Review
- SARS-CoV-2 ORF10 suppresses the antiviral innate immune response by degrading MAVS through mitophagy.Cellular & molecular immunology · 2022Article
- RNA regulatory mechanisms that control antiviral innate immunity.Immunological reviews · 2021Review
- MAVS: A Two-Sided CARD Mediating Antiviral Innate Immune Signaling and Regulating Immune Homeostasis.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The monomer-to-filament transition of MAVS is essential for the RIG-I/MDA5-mediated antiviral signaling. In quiescent cells, monomeric MAVS is under strict regulation for preventing its spontaneous aggregation, which would result in dysregulated interferon (IFN-α/β) production and autoimmune diseases like systemic lupus erythematosus. However, the detailed mechanism by which MAVS is kept from spontaneous aggregation remains largely unclear. Here, we show that upstream open reading frames (uORFs) within the MAVS transcripts exert a post-transcriptional regulation for preventing MAVS spontaneous aggregation and auto-activation. Mechanistically, we demonstrate that uORFs are cis-acting elements initiating leaky ribosome scanning of the downstream ORF codons, thereby repressing the full-length MAVS translation. We further uncover that endogenous MAVS generated from the uORF-deprived transcript spontaneously aggregates, triggering the Nix-mediated mitophagic clearance of damaged mitochondria and aggregated MAVS. Our findings reveal the uORF-mediated quantity and quality control of MAVS, which prevents aberrant protein aggregation and maintains innate immune homeostasis.
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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.