ArticleFrontiers in cellular and infection microbiology2024
ZIKV prM hijacks PIM1 kinase for phosphorylation to prevent ubiquitin-mediated degradation and facilitate viral replication.
Article in Frontiers in cellular and infection microbiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Identification of UL3.5 as a novel substrate of DPV US3 kinase whose phosphorylation at Ser64/Ser84 enhances protein stability and promotes viral release, and cell-to-cell spread.Poultry science · 2026Article
- Host-specific ubiquitination of prM orchestrates ESCRT recruitment to mediate efficient Japanese Encephalitis Virus assembly in vertebrates.PLoS pathogens · 2026Article
- In Silico Identification of Lepiotaprocerin C as a Promising PIM-1 Kinase Inhibitor: An Integrated Docking, Molecular Dynamics, MM/PBSA, QSAR, and ADMET Study.Bioinformatics and biology insights · 2026Article
- Zika virus and host protein interactions for understanding molecular mechanisms of pathogenesis and therapeutic development.Frontiers in cellular and infection microbiology · 2026Review
- The roles of post-translational modifications in the pathogenesis of RNA viruses: allies or adversaries?Frontiers in microbiology · 2026Review
- IKZF1 exacerbates the inflammatory response by epigenetically modulating mitochondrial function following acute peritonitis.Frontiers in immunology · 2025Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Viral infection usually stimulates a variety of host cell factors to modulate the life cycle of the virus. PIM1, a serine/threonine protein kinase widely involved in cell proliferation, survival, differentiation and apoptosis, was recently reported to be upregulated by Zika virus (ZIKV) infection. However, how ZIKV-PIM1 interactions affect the viral life cycle are not fully understood. Methods and results: Here, we demonstrated that ZIKV replication was suppressed by the PIM1 kinase inhibitor SGI-1776 in both Discussion: These findings revealed PIM1 as a critical host factor that is advantageous to ZIKV and revealed that targeting the PIM1‒prM axis is a conducive strategy for controlling ZIKV infection.
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