ArticleJournal of virology2008
Cleavage of poly(A)-binding protein by poliovirus 3C proteinase inhibits viral internal ribosome entry site-mediated translation.
Article in Journal of virology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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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.
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Who cites it
43 citing papers in PubMed, 56 citations in OpenAlex.
- Review
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- Dosa: A method to covalently barcode proteins for high-throughput biochemistry.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Dosa: A method to covalently barcode proteins for high throughput biochemistry.bioRxiv : the preprint server for biology · 2025Article
- Canine parvovirus NS1 induces host translation shutoff by reducing mTOR phosphorylation.Journal of virology · 2025Article
- Enterovirus-D68 - A Reemerging Non-Polio Enterovirus that Causes Severe Respiratory and Neurological Disease in Children.Frontiers in virology (Lausanne, Switzerland) · 2024Article
- 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
- Uncovering targets of the Leader protease: Linking RNA-mediated pathways and antiviral defense.Wiley interdisciplinary reviews. RNA · 2021Review
- RNA-Binding Proteins at the Host-Pathogen Interface Targeting Viral Regulatory Elements.Viruses · 2021Article
- Running With Scissors: Evolutionary Conflicts Between Viral Proteases and the Host Immune System.Frontiers in immunology · 2021Review
- Seneca Valley Virus 3CPathogens (Basel, Switzerland) · 2020Article
- Article
- Strand-specific affinity of host factor hnRNP C1/C2 guides positive to negative-strand ratio in Coxsackievirus B3 infection.RNA biology · 2019Article
- Stimulation of the Internal Ribosome Entry Site (IRES)-Dependent Translation of Enterovirus 71 by DDX3X RNA Helicase and Viral 2A and 3C Proteases.Frontiers in microbiology · 2018Article
- Cleavage of poly(A)-binding protein by duck hepatitis A virus 3C protease.Scientific reports · 2017Article
- Polypyrimidine tract-binding protein (PTB) and PTB-associated splicing factor in CVB3 infection: an ITAF for an ITAF.Nucleic acids research · 2017Article
- A Novel Enterovirus 71 (EV71) Virulence Determinant: The 69th Residue of 3C Protease Modulates Pathogenicity.Frontiers in cellular and infection microbiology · 2017Article
- Rhinovirus 16 2A Protease Affects Nuclear Localization of 3CD during Infection.Journal of virology · 2016Article
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The two enteroviral proteinases, 2A proteinase (2A(pro)) and 3C proteinase (3C(pro)), induce host cell translation shutoff in enterovirus-infected cells by cleaving canonical translation initiation factors. Cleavage of poly(A)-binding protein (PABP) by 3C(pro) has been shown to be a necessary component for host translation shutoff. Here we show that 3C(pro) inhibits cap-independent translation mediated by the poliovirus internal ribosome entry site (IRES) in a dose-dependent manner in HeLa translation extracts displaying cap-poly(A) synergy. This effect is independent of the stimulatory effect of 2A(pro) on IRES translation, and 3C(pro)-induced translation inhibition can be partially rescued by addition of recombinant PABP in vitro. 3C(pro) inhibits IRES translation on transcripts containing or lacking poly(A) tails, suggesting that cleavage of PABP and IRES trans-activating factors polypyrimidine tract-binding protein and poly r(C)-binding protein 2 may also be important for inhibition. Expression of 3C(pro) cleavage-resistant PABP in cells increased translation of nonreplicating viral minigenome reporter RNAs during infection and also delayed and reduced virus protein synthesis from replicating RNA. Further, expression of cleavage-resistant PABP in cells reduced the accumulation of viral RNA and the output of infectious virus. These results suggest that cleavage of PABP contributes to viral translation shutoff that is required for the switch from translation to RNA replication.
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Registered trials
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