ArticleViruses2023
BAK-Mediated Pyroptosis Promotes Japanese Encephalitis Virus Proliferation in Porcine Kidney 15 Cells.
Article in Viruses, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- 25-Hydroxycholesterol Restricts Japanese Encephalitis Virus via Metabolic Suppression of the SREBP2-Mediated Signaling Axis.Microorganisms · 2026Article
- Transcriptomic insights into the neuropathogenic and immune response alterations in mouse neurons challenged with west nile and japanese encephalitis viruses.Virology journal · 2026Article
- Japanese encephalitis virus activates the NLRP3/caspase-1/GSDMD signaling pathway in dopaminergic neurons.PLoS neglected tropical diseases · 2026Article
- Host Factor Rab4b PromotesMicroorganisms · 2024Article
- Monkeypox virus infection of human astrocytes causes gasdermin B cleavage and pyroptosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Preparation and characterization of monoclonal antibodies against porcine gasdermin D protein.Applied microbiology and biotechnology · 2024Article
- Advances in research on the impact and mechanisms of pathogenic microorganism infections on pyroptosis.Frontiers in microbiology · 2024Review
- Japanese encephalitis virus infection induces mitochondrial-mediated apoptosis through the proapoptotic protein BAX.Frontiers in microbiology · 2024Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As a zoonotic virus, Japanese Encephalitis virus (JEV) poses a serious threat to human health and the breeding industry. Regarding the mechanism and complications of tissue inflammation caused by JEV, such as encephalitis and orchitis, there is no effective drug treatment currently, and the mechanism of occurrence has not been thoroughly studied. Therefore, it is necessary to study the mechanism of the inflammatory pathway caused by JEV. As one of the key proteins regulating cell death, BCL2 antagonist/killer (BAK) is also a necessary prerequisite for the release of cellular inflammatory factors. We found that after JEV infection, BAK-knockdown cells died less than normal cells, and the transcription levels of inflammatory factors such as
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Registered trials
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