ArticleNature communications2020
MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling.
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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.
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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
- MG53 Coordinates Macrophage Polarization and Neuroimmune Coupling to Promote Corneal Nerve Regeneration via the MPEG1-MVP-STAT6 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- TRIM Expression and Its Association With Disease Activity in Systemic Lupus Erythematosus.The Kaohsiung journal of medical sciences · 2026Article
- Machine Learning and Experimental Verification Identify Anti-Influenza Natural Products.International journal of molecular sciences · 2026Article
- Deciphering Lipid Metabolic Landscape of Sorafenib-Treated Hepatocellular Carcinoma by Mass Spectrometry Imaging and Transcriptomics.Biomolecules · 2026Article
- Mitsugumin 53 protects against smoke inhalation lung injury via suppressing the proinflammatory response in a rat model.Free radical biology & medicine · 2026Article
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- MG53 in Early Skeletal Muscle Stem Cell Activation: Implications for Aged Muscle Regeneration.Cells · 2026Review
- MG53 protects against intestinal inflammation by inhibiting NLRP3 inflammasome activation.Frontiers in pharmacology · 2026Article
- MG53 protects against septic cardiac dysfunction by ubiquitinating ATF2.Journal of advanced research · 2026Article
- Intracellular Calcium as a Regulator of Polarization and Target Reprogramming of Macrophages.International journal of molecular sciences · 2025Review
- Unravelling distinct patterns of metagenomic surveillance and respiratory microbiota between two P1 genotypes ofEmerging microbes & infections · 2025Article
- Antimicrobial peptide LL-37 increases rhinovirus-induced interferon β expression in human airway epithelial cells through a CaBiochemistry and biophysics reports · 2025Article
- Anti-TRIM72 Autoantibodies in Idiopathic Inflammatory Myopathies.medRxiv : the preprint server for health sciences · 2025Article
- Nuclear AGO2 supports influenza A virus replication through type-I interferon regulation.Nucleic acids research · 2025Article
- The Relationship Between Serum MG53 Levels and the Presence of Metabolic Syndrome and Its Components.Medicina (Kaunas, Lithuania) · 2025Article
- Mitsugumin 53 Inhibits Angiogenesis Through Regulating Focal Adhesion Turnover and Tip Cell Formation.Journal of cellular and molecular medicine · 2025Article
- Recombinant human mitsugumin 53: a potential therapeutic agent for multiple diseases.Frontiers in pharmacology · 2025Review
- Trim72 is a major host factor protecting against lethal Candida albicans infection.PLoS pathogens · 2024Article
- FBXL19 in endothelial cells protects the heart from influenza A infection by enhancing antiviral immunity and reducing cellular senescence programs.American journal of physiology. Heart and circulatory physiology · 2024Article
- Gasdermin D promotes influenza virus-induced mortality through neutrophil amplification of inflammation.Nature communications · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
TRIM family proteins play integral roles in the innate immune response to virus infection. MG53 (TRIM72) is essential for cell membrane repair and is believed to be a muscle-specific TRIM protein. Here we show human macrophages express MG53, and MG53 protein expression is reduced following virus infection. Knockdown of MG53 in macrophages leads to increases in type I interferon (IFN) upon infection. MG53 knockout mice infected with influenza virus show comparable influenza virus titres to wild type mice, but display increased morbidity accompanied by more accumulation of CD45+ cells and elevation of IFNβ in the lung. We find that MG53 knockdown results in activation of NFκB signalling, which is linked to an increase in intracellular calcium oscillation mediated by ryanodine receptor (RyR). MG53 inhibits IFNβ induction in an RyR-dependent manner. This study establishes MG53 as a new target for control of virus-induced morbidity and tissue injury.
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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.