ArticleProceedings of the National Academy of Sciences of the United States of America2024
PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Review
- PAWR augments anti-RNA viral innate immunity by promoting the PIM2-XBP1s-RIG-I signaling axis.Nature communications · 2026Article
- USP17L13 Enhances Influenza a Virus Replication by Mediating the Degradation of RIG-I and MDA5.Viruses · 2026Article
- Bioinformatics analysis ofTranslational cancer research · 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
- The emerging role of E3 ubiquitin ligases and deubiquitinases in metabolic dysfunction-associated steatotic liver disease.Journal of translational medicine · 2025Review
- Determination of Protein Ubiquitination After Protein Denaturation in Virus-Host Interactions.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Sec10 negatively regulates antiviral immunity by downregulating NRF2-ATF4-RIG-I axis.International journal of biological sciences · 2025Article
- PBLD enhances antiviral innate immunity by promoting the p53-USP4-MAVS signaling axis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
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Authors and funding
13 authors.
Funding
Abstract
Phenazine biosynthesis-like domain-containing protein (PBLD) has been reported to be involved in the development of many cancers. However, whether PBLD regulates innate immune responses and viral replication is unclear. In this study, although it was found that the activity of PBLD extends to other PRRs, we focused on the RLR pathway activated via the p53-USP4-MAVS axis in response to virus infections. We found that PBLD deubiquitinates and stabilizes MAVS through ubiquitin-specific protease 4 (USP4) to promote antiviral innate immunity. Mechanistically, PBLD activates the transcription of USP4 via the upregulation of p53. USP4, which is a MAVS-interacting protein, substantially stabilizes the MAVS protein by deconjugating K48-linked ubiquitination chains from the MAVS protein at Lys461 during RNA virus infection. Most intriguingly, RNA virus-infected primary macrophages (peritoneal macrophages, PMs, and bone marrow-derived macrophages, BMDMs) and internal organ cells (lung and liver) from PBLD-deficient mice suppress the IFN-I response and promote viral replication. Notably, PBLD-deficient mice are more susceptible to RNA virus infection than their wild-type littermates. Our findings highlight a unique function of PBLD in antiviral innate immunity through the p53-USP4-MAVS signaling, providing a preliminary basis for research on PBLD as a target molecule for treating RNA virus infection.
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