ArticleNature communications2025
Phenazine biosynthesis-like domain-containing protein (PBLD) and Cedrelone promote antiviral immune response by activating NF-ĸB.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed.
- PAWR augments anti-RNA viral innate immunity by promoting the PIM2-XBP1s-RIG-I signaling axis.Nature communications · 2026Article
- PBLD Orchestrates the STING-Mediated Antiviral Immune Response and Autoimmune Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- Sec10 negatively regulates antiviral immunity by downregulating NRF2-ATF4-RIG-I axis.International journal of biological sciences · 2025Article
- Natural mutations in key NLS amino acids regulate nucleoplasmic shuttling and replication efficiency in PRRSV.Frontiers in microbiology · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
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Abstract
Phenazine biosynthesis-like domain-containing protein (PBLD) and Cedrelone have been identified as tumor suppressors. However, their roles in virus infection remain unclear. Here, we demonstrate that PBLD upregulates the type I interferon (IFN-I) response through activating NF-kappaB (NF-κB) signaling pathway to resist viral infection in cells and mice. Mechanistically, PBLD activates NF-κB signaling pathway during viral infection via blocking tripartite motif containing 21 (TRIM21)-mediated phosphorylated inhibitory kappa B kinase beta (IKKβ) degradation. Furthermore, we show Cedrelone inhibits viral replication by increasing the PBLD protein expression and subsequently activating NF-κB-mediated IFN-I response. Furthermore, the therapeutic potential of Cedrelone lies in its ability to enhance antiviral immunity in primary macrophages and to promote survival and reduce lung tissue damage in HSV-1-infected mice in a PBLD-dependent manner. Consequently, our findings provide a potential combination model that targets PBLD for Cedrelone antiviral drug therapy, potentially paving the way for the development of broad-spectrum antiviral agents.
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Registered trials
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