ArticleJournal of virology2019
The Leader Protein of Theiler's Virus Prevents the Activation of PKR.
Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Completion of the 5' end of the porcine teschovirus genome reveals a functional S-segment and enables reverse genetics.Journal of virology · 2026Article
- Cardiovirus-Mediated PKR inhibition results from nucleocytoplasmic trafficking disruption.PLoS pathogens · 2025Article
- The leader proteins of Theiler's virus and Boone cardiovirus use a combination of short linear motifs (SLiMs) to target RSK kinases to the nuclear pore complex.Journal of virology · 2025Article
- The Interplay Between Therapeutic Self-Amplifying RNA and the Innate Immune System: Balancing Efficiency and Reactogenicity.International journal of molecular sciences · 2025Review
- Article
- IFN alpha inducible protein 27 (IFI27) acts as a positive regulator of PACT-dependent PKR activation after RNA virus infections.PLoS pathogens · 2025Article
- Controlling reactogenicity while preserving immunogenicity from a self-amplifying RNA vaccine by modulating nucleocytoplasmic transport.NPJ vaccines · 2025Article
- Picornavirus security proteins promote the release of extracellular vesicle enclosed viruses via the modulation of host kinases.PLoS pathogens · 2024Article
- SARS-CoV-2 nucleocapsid protein inhibits the PKR-mediated integrated stress response through RNA-binding domain N2b.PLoS pathogens · 2023Article
- Biomolecular phase separation in stress granule assembly and virus infection.Acta biochimica et biophysica Sinica · 2023Article
- IFNAR signaling of neuroectodermal cells is essential for the survival of C57BL/6 mice infected with Theiler's murine encephalomyelitis virus.Journal of neuroinflammation · 2023Article
- A little less aggregation a little more replication: Viral manipulation of stress granules.Wiley interdisciplinary reviews. RNA · 2023Review
- Move and countermove: the integrated stress response in picorna- and coronavirus-infected cells.Current opinion in immunology · 2022Review
- Cardiovirus leader proteins retarget RSK kinases toward alternative substrates to perturb nucleocytoplasmic traffic.PLoS pathogens · 2022Article
- A case of convergent evolution: Several viral and bacterial pathogens hijack RSK kinases through a common linear motif.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mechanism of herpesvirus protein kinase UL13 in immune escape and viral replication.Frontiers in immunology · 2022Review
- PKR activity modulation by phosphomimetic mutations of serine residues located three aminoacids upstream of double-stranded RNA binding motifs.Scientific reports · 2021Article
- Coronavirus Endoribonuclease Ensures Efficient Viral Replication and Prevents Protein Kinase R Activation.Journal of virology · 2021Article
- Inhibition of PKR by Viruses.Frontiers in microbiology · 2021Review
- Induction of UPR Promotes Interferon Response to Inhibit PRRSV ReplicationFrontiers in microbiology · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leader (L) proteins encoded by cardioviruses are multifunctional proteins that contribute to innate immunity evasion. L proteins of Theiler's murine encephalomyelitis virus (TMEV), Saffold virus (SAFV), and encephalomyocarditis virus (EMCV) were reported to inhibit stress granule assembly in infected cells. Here, we show that TMEV L can act at two levels in the stress granule formation pathway: on the one hand, it can inhibit sodium arsenite-induced stress granule assembly without preventing eIF2α phosphorylation and, thus, acts downstream of eIF2α; on the other hand, it can inhibit eucaryotic translation initiation factor 2 alpha kinase 2 (PKR) activation and the consequent PKR-mediated eIF2α phosphorylation. Interestingly, coimmunostaining experiments revealed that PKR colocalizes with viral double-stranded RNA (dsRNA) in cells infected with L-mutant viruses but not in cells infected with the wild-type virus. Furthermore, PKR coprecipitated with dsRNA from cells infected with L-mutant viruses significantly more than from cells infected with the wild-type virus. These data strongly suggest that L blocks PKR activation by preventing the interaction between PKR and viral dsRNA. In infected cells, L also rendered PKR refractory to subsequent activation by poly(I·C). However, no interaction was observed between L and either dsRNA or PKR. Taken together, our results suggest that, unlike other viral proteins, L indirectly acts on PKR to negatively regulate its responsiveness to dsRNA.
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