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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay

Published on: May 3, 2018

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JNK kinase regulates phosphorylation of HCoV-229E nucleocapsid protein

Yannick Brüggemann1, Toni Luise Meister2,3,4,5, Natalie Heinen2

  • 1Department of Molecular and Medical Virology, Ruhr University Bochum, Bochum, Germany. yannick.brueggemann@ruhr-uni-bochum.de.

Npj Viruses
|September 18, 2025
PubMed

Insights

The c-Jun N-terminal kinase (JNK) pathway is crucial for human coronavirus (HCoV) replication. Inhibiting JNK effectively blocks HCoV-229E and SARS-CoV-2, suggesting JNK inhibitors as potential broad-spectrum antivirals.

Area of Science:

  • Virology
  • Molecular Biology
  • Immunology

Background:

  • Human coronaviruses (HCoV) pose significant health challenges, necessitating the identification of host factors for therapeutic targeting.
  • Mitogen-activated protein kinases (MAPKs), particularly c-Jun N-terminal kinases (JNK), are involved in cellular stress responses, but their role in HCoV replication is not well understood.

Purpose of the Study:

  • To investigate the role of the JNK signaling pathway in the replication cycle of human coronaviruses.
  • To determine if JNK pathway activation is essential for HCoV replication and if it represents a viable therapeutic target.

Main Methods:

  • Live-cell microscopy
  • Quantitative immunofluorescence
  • Immunoblotting
  • Pharmacological inhibition of JNK kinase activity

Main Results:

  • JNK signaling is specifically activated during HCoV-229E infection.
  • JNK mediates the phosphorylation of the viral nucleocapsid (N) protein, a critical step in viral replication.
  • Inhibition of JNK kinase activity significantly reduced HCoV-229E and SARS-CoV-2 replication.

Conclusions:

  • The JNK pathway is essential for HCoV replication, highlighting its role in host-pathogen interactions.
  • Targeting JNK kinase activity with pharmacological inhibitors shows promise as a broad-spectrum antiviral strategy against coronaviruses, including SARS-CoV-2.

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