ArticleNature communications2025
PWWP3A disrupts the assembly of VISA/MAVS signalosome to inhibit innate immune response against RNA viruses.
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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Who cites it
5 citing papers in PubMed.
- ALOX15 orchestrates mitochondrial antiviral immunity and serves as a host target for anti-influenza therapy.Nature immunology · 2026Article
- Review
- The mitochondrial GTPase ERAL1 inhibits HBV replication by triggering the MAVS signaling cascade.Journal of translational medicine · 2026Article
- A photodynamically activated nanoplatform relieves glucose-driven immunosuppression to potentiate STING immunotherapy in triple-negative breast cancer.Materials today. Bio · 2026Article
- Integration of RNA Editing into Multiomics Machine Learning Models for Predicting Drug Responses in Breast Cancer Patients.Biomedicines · 2026Article
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12 authors.
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Abstract
VISA/MAVS is crucial in antiviral innate immunity. Upon RNA virus infection, VISA recruits TBK1 via TRAFs to mitochondria, inducing IRF3 phosphorylation and type I interferons. However, TBK1 recruitment mechanisms via individual TRAFs are unclear. Here, we reveal that PWWP domain-containing 3A (PWWP3A) serves as a negative regulator of RNA virus-triggered signaling. During viral infection, PWWP3A translocates from nucleus to the mitochondria, competing with TRAF6 for binding to VISA, thereby impeding the recruitment of TBK1 and inhibiting IRF3 activation. However, the extent of PWWP3A-mediated inhibition is regulated by the E3 ligase PJA2, which induces PWWP3A degradation post-infection, highlighting the intricate regulatory network in antiviral immunity. Consistently, PWWP3A deficiency enhances antiviral responses, and Pwwp3a
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