ArticleJournal of virology2012
Site-specific cleavage of the host poly(A) binding protein by the encephalomyocarditis virus 3C proteinase stimulates viral replication.
Article in Journal of virology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 32 citations in OpenAlex.
- Binding of Glycyl-tRNA synthetase to Mengovirus RNA stimulates translation.Nucleic acids research · 2026Article
- Virulence determinant of Senecavirus A: 3C protein functions as a protease to cleave viral polyprotein and host factors.Virulence · 2025Review
- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- When Poly(A) Binding Proteins Meet Viral Infections, Including SARS-CoV-2.Journal of virology · 2022Review
- Minding the message: tactics controlling RNA decay, modification, and translation in virus-infected cells.Genes & development · 2022Review
- The game between host antiviral innate immunity and immune evasion strategies of senecavirus A - A cell biological perspective.Frontiers in immunology · 2022Review
- Innate immune evasion mediated by picornaviral 3C protease: Possible lessons for coronaviral 3C-like protease?Reviews in medical virology · 2021Review
- Nervous Necrosis Virus Coat Protein Mediates Host Translation Shutoff through Nuclear Translocalization and Degradation of Polyadenylate Binding Protein.Journal of virology · 2021Article
- Foot-and-Mouth Disease Virus Inhibits RIP2 Protein Expression to Promote Viral Replication.Virologica Sinica · 2021Article
- Running With Scissors: Evolutionary Conflicts Between Viral Proteases and the Host Immune System.Frontiers in immunology · 2021Review
- Duck Hepatitis A Virus Type 1 Induces eIF2α Phosphorylation-Dependent Cellular Translation ShutoffFrontiers in microbiology · 2021Article
- eIF4G-driven translation initiation of downstream ORFs in mammalian cells.Nucleic acids research · 2020Article
- The diversity, plasticity, and adaptability of cap-dependent translation initiation and the associated machinery.RNA biology · 2020Review
- The role of host eIF2α in viral infection.Virology journal · 2020Review
- Seneca Valley Virus 3CPathogens (Basel, Switzerland) · 2020Article
- Structural Biology of the Enterovirus Replication-Linked 5'-Cloverleaf RNA and Associated Virus Proteins.Microbiology and molecular biology reviews : MMBR · 2020Review
- Translational Control in Virus-Infected Cells.Cold Spring Harbor perspectives in biology · 2019Review
- Messenger RNAs of Yeast Virus-Like Elements Contain Non-templated 5' Poly(A) Leaders, and Their Expression Is Independent of eIF4E and Pab1.Frontiers in microbiology · 2019Article
- Picornavirus 2A protease regulates stress granule formation to facilitate viral translation.PLoS pathogens · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Although picornavirus RNA genomes contain a 3'-terminal poly(A) tract that is critical for their replication, the impact of encephalomyocarditis virus (EMCV) infection on the host poly(A)-binding protein (PABP) remains unknown. Here, we establish that EMCV infection stimulates site-specific PABP proteolysis, resulting in accumulation of a 45-kDa N-terminal PABP fragment in virus-infected cells. Expression of a functional EMCV 3C proteinase was necessary and sufficient to stimulate PABP cleavage in uninfected cells, and bacterially expressed 3C cleaved recombinant PABP in vitro in the absence of any virus-encoded or eukaryotic cellular cofactors. N-terminal sequencing of the resulting C-terminal PABP fragment identified a 3C(pro) cleavage site on PABP between amino acids Q437 and G438, severing the C-terminal protein-interacting domain from the N-terminal RNA binding fragment. Single amino acid substitution mutants with changes at Q437 were resistant to 3C(pro) cleavage in vitro and in vivo, validating that this is the sole detectable PABP cleavage site. Finally, while ongoing protein synthesis was not detectably altered in EMCV-infected cells expressing a cleavage-resistant PABP variant, viral RNA synthesis and infectious virus production were both reduced. Together, these results establish that the EMCV 3C proteinase mediates site-specific PABP cleavage and demonstrate that PABP cleavage by 3C regulates EMCV replication.
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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.