ArticleJournal of virology2014
Encephalomyocarditis virus leader is phosphorylated by CK2 and syk as a requirement for subsequent phosphorylation of cellular nucleoporins.
Article in Journal of virology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- Insights from structural studies of the cardiovirus 2A protein.Bioscience reports · 2022Review
- Review
- Protein kinase CK2: a potential therapeutic target for diverse human diseases.Signal transduction and targeted therapy · 2021Review
- Innate Immune Detection of Cardioviruses and Viral Disruption of Interferon Signaling.Frontiers in microbiology · 2018Review
- Differential Disruption of Nucleocytoplasmic Trafficking Pathways by Rhinovirus 2A Proteases.Journal of virology · 2017Article
- Intracellular localization of Saffold virus Leader (L) protein differs in Vero and HEp-2 cells.Emerging microbes & infections · 2016Article
- Cardiovirus Leader proteins bind exportins: Implications for virus replication and nucleocytoplasmic trafficking inhibition.Virology · 2016Article
- Three cardiovirus Leader proteins equivalently inhibit four different nucleocytoplasmic trafficking pathways.Virology · 2015Article
- Review
- Solution structures of Mengovirus Leader protein, its phosphorylated derivatives, and in complex with nuclear transport regulatory protein, RanGTPase.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Binding interactions between the encephalomyocarditis virus leader and protein 2A.Journal of virology · 2014Article
- Induction and suppression of innate antiviral responses by picornaviruses.Cytokine & growth factor reviews · 2014Review
- AMP-activated protein kinase phosphorylates EMCV, TMEV and SafV leader proteins at different sites.Virology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Encephalomyocarditis virus and Theilovirus are species in the Cardiovirus genus of the Picornaviridae family. For all cardioviruses, the viral polyprotein is initiated with a short Leader (L) protein unique to this genus. The nuclear magnetic resonance (NMR) structure of LE from encephalomyocarditis virus (EMCV) has been determined. The protein has an NH2-proximal CHCC zinc finger, a central linker, and a contiguous, highly acidic motif. The theiloviruses encode the same domains, with one or two additional, COOH-proximal domains, characteristic of the human Saffold viruses (SafV) and Theiler's murine encephalomyelitis viruses (TMEV), respectively. The expression of a cardiovirus L, in recombinant form, or during infection/transfection, triggers an extensive, cell-dependent, antihost phosphorylation cascade, targeting nucleoporins (Nups) that form the hydrophobic core of nuclear pore complexes (NPC). The consequent inhibition of active nucleocytoplasmic trafficking is potent and prevents the host from mounting an effective antiviral response. For this inhibition, the L proteins themselves must be phosphorylated. In cells (extracts or recombinant form), LE was shown to be phosphorylated at Thr47 and Tyr41. The first reaction (Thr47), catalyzed by casein kinase 2 (CK2), is an obligatory precedent to the second event (Tyr41), catalyzed by spleen tyrosine kinase (Syk). Site mutations in LE, or kinase-specific inhibitors, prevented LE phosphorylation and subsequent Nup phosphorylation. Parallel experiments with LS (SafV-2) and LT (TMEV BeAn) proteins confirmed the general cardiovirus requirement for L phosphorylation, but CK2 was not the culpable kinase. It is likely that LS and LT are both activated by alternative kinases in different cell types, probably reactive within the Theilo-specific domains. IMPORTANCE An understanding of the diverse methods used by viruses to interfere with cellular processes is important because they can teach us how to control virus infections. This report shows how viruses in the same genus use different cellular enzymes to phosphorylate their proteins. If these processes are interfered with, the viruses are severely disabled.
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