ArticleCell reports2013
UBXN1 interferes with Rig-I-like receptor-mediated antiviral immune response by targeting MAVS.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 70 citations in OpenAlex.
- Unanchored ubiquitin chains promote the non-canonical inflammasome via UBXN1.Research square · 2026Article
- FMDV 3A cooperates with PDCD10 to promote FMDV replication by inhibiting VISA-mediated innate immunity.Journal of virology · 2025Article
- Exploiting host kinases to combat dengue virus infection and disease.Antiviral research · 2025Review
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Nature immunology · 2024Article
- Article
- UBXN9 governs GLUT4-mediated spatial confinement of RIG-I-like receptors and signaling.Research square · 2024Article
- UBXN1 promotes liver tumorigenesis by regulating mitochondrial homeostasis.Journal of translational medicine · 2024Article
- Identification of common genes of rhinovirus single/double‑stranded RNA‑induced asthma deterioration by bioinformatics analysis.Experimental and therapeutic medicine · 2024Article
- UBXN1 maintains ER proteostasis and represses UPR activation by modulating translation.EMBO reports · 2024Article
- UBR5 promotes antiviral immunity by disengaging the transcriptional brake on RIG-I like receptors.Nature communications · 2024Article
- MAVI1, an endoplasmic reticulum-localized microprotein, suppresses antiviral innate immune response by targeting MAVS on mitochondrion.Science advances · 2023Article
- WDR77 inhibits prion-like aggregation of MAVS to limit antiviral innate immune response.Nature communications · 2023Article
- Article
- Cooperative assembly of p97 complexes involved in replication termination.Nature communications · 2022Article
- Regulation of antiviral innate immune signaling and viral evasion following viral genome sensing.Experimental & molecular medicine · 2021Review
- A Combined mRNA- and miRNA-Sequencing Approach Reveals miRNAs as Potential Regulators of the Small Intestinal Transcriptome in Celiac Disease.International journal of molecular sciences · 2021Article
- UBX Domain Protein 6 Positively Regulates JAK-STAT1/2 Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- Article
- Foot-and-mouth disease virus VP1 target the MAVS to inhibit type-I interferon signaling and VP1 E83K mutation results in virus attenuation.PLoS pathogens · 2020Article
- Decanoic acid inhibits mTORC1 activity independent of glucose and insulin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
RNA viruses are sensed by RIG-I-like receptors (RLRs), which signal through a mitochondria-associated adaptor molecule, MAVS, resulting in systemic antiviral immune responses. Although RLR signaling is essential for limiting RNA virus replication, it must be stringently controlled to prevent damage from inflammation. We demonstrate here that among all tested UBX-domain-containing protein family members, UBXN1 exhibits the strongest inhibitory effect on RNA-virus-induced type I interferon response. UBXN1 potently inhibits RLR- and MAVS-induced, but not TLR3-, TLR4-, or DNA-virus-induced innate immune responses. Depletion of UBXN1 enhances virus-induced innate immune responses, including those resulting from RNA viruses such as vesicular stomatitis, Sendai, West Nile, and dengue virus infection, repressing viral replication. Following viral infection, UBXN1 is induced, binds to MAVS, interferes with intracellular MAVS oligomerization, and disrupts the MAVS/TRAF3/TRAF6 signalosome. These findings underscore a critical role of UBXN1 in the modulation of a major antiviral signaling pathway.
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What OpenQuestion holds
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.