ArticleNpj viruses2025
JNK kinase regulates phosphorylation of HCoV-229E nucleocapsid protein.
Article in Npj viruses, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed.
- Tetramethylpyrazine modulates the Nrf2/JNK axis to intervene in ferroptosis and neuroinflammation after spinal cord injury: an integrated perspective from antioxidant to regenerative therapy.Molecular biology reports · 2026Review
- SARS-CoV-2 membrane protein recruits PP2A to dephosphorylate the nucleocapsid and promote virion production.Journal of biomedical science · 2026Article
- Chemical modulation of the unfolded protein response reveals an antiviral role for the PERK pathway in human coronavirus 229E infection.RSC chemical biology · 2026Article
- Exacerbations and Management of Asthma in Viral Lower Respiratory Tract Infections: The Significance of Immunoglobulin E.Immunity, inflammation and disease · 2026Review
- Intramolecular loops control SARS-CoV-2 nucleocapsid protein self-association and nucleic acid binding dependent on phosphorylation.bioRxiv : the preprint server for biology · 2026Article
- Intersection of inflammation and viral replication: the central role of MAPK signaling in viral respiratory infections.Frontiers in microbiology · 2025Review
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Identifying common host factors essential for the replication cycles of human coronaviruses (HCoV) could help uncover potential therapeutic targets. Mitogen-activated protein kinases (MAPKs) regulate critical cellular signaling pathways. Among them, c-Jun N-terminal kinases (JNK) are activated in response to diverse environmental stresses, including viral infections. However, the relevance of the JNK pathway for host responses and replication of HCoV infections has remained elusive. Using live-cell microscopy, quantitative immunofluorescence and immunoblotting, we found that JNK is specifically activated in cells infected with HCoV-229E and plays a crucial role in mediating the phosphorylation of the viral nucleocapsid (N) protein, an essential step required during the viral replication cycle. Consequently, pharmacological inhibition of JNK kinase activity impeded HCoV-229E as well as SARS-CoV-2 infection. Given the conservation of phosphorylation sites within the nucleocapsid protein across coronaviruses, inhibitors targeting these N protein kinases, such as JNK, may hold therapeutic promise as broad-spectrum CoV antivirals.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.