ArticlePLoS pathogens2025
RNF213 regulates blood‒brain barrier integrity by targeting TRAF3 for type I interferon activation during A. baumannii infection.
Article in PLoS pathogens, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Synergetic attenuated inflammatory response and increased apoptosis confer high pathogenicity ofVirulence · 2026Article
- An Rnf213-deficient hypoperfusion model reveals Moyamoya-relevant neurovascular remodeling.Angiogenesis · 2026Article
- RNF213 Is an Interferon-Stimulated Gene That Targets Influenza A Virus NP and Activates MDA5 to Restrict Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Multi-omics profiling of gut microbiota and host transcriptome identifies diagnostic signatures and mechanistic links in moyamoya disease.BMC microbiology · 2026Article
- Ring finger protein 213 regulates B-cell receptor signaling, metabolism, and development in B lymphocytes.Signal transduction and targeted therapy · 2026Article
- Article
- Bergeyella cardium variant induces a unique cytoplasmic vacuolization cell death floatptosis in macrophage.Cell discovery · 2025Article
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Authors and funding
8 authors.
Funding
Abstract
RNF213 is the first identified susceptibility gene for moyamoya disease, and the encoded protein was recently recognized as a key antimicrobial protein. However, the function of RNF213 in host defense against brain infection remains unclear. Here, we show that increased expression of Rnf213 is significantly regulated by interferon alpha/beta receptor (IFNAR) signaling during bacterial infection and ligand stimulation. RNF213 deficiency impairs type I interferon (IFN-I) production and decreases the expression of interferon-stimulated genes (ISGs) in response to IFN-β stimulation and Acinetobacter baumannii infection. Mechanistically, RNF213 interacts with TRAF3 and mediates the K27-linked polyubiquitination of TRAF3 at K160. RNF213 regulates the expression of the endothelial tight junction-related genes Claudin-5, Occludin, and Pecam1 via IFN-I signaling. Furthermore, RNF213 deficiency in nonimmune cells increases blood‒brain barrier (BBB) disruption and the bacterial load in the brain parenchyma in response to A. baumannii infection due to impaired IFN-I signaling. Thus, RNF213 mediates BBB integrity by targeting TRAF3 for the regulation of IFN-I signaling against bacterial brain infection. Our study principally provides a deeper understanding of the function of RNF213 and reveals potential therapeutic targets against bacterial brain infection and moyamoya disease.
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