ArticleVirology2011
Mutational analysis of the EMCV 2A protein identifies a nuclear localization signal and an eIF4E binding site.
Article in Virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 35 citations in OpenAlex.
- Modulation of Ire1-Xbp1 Defense Pathway in Encephalomyocarditis Virus-Infected HeLa Cells.Viruses · 2025Article
- Comprehensive Elucidation of the Role of L and 2A Security Proteins on Cell Death during EMCV Infection.Viruses · 2024Article
- Host Subcellular Organelles: Targets of Viral Manipulation.International journal of molecular sciences · 2024Review
- Encephalomyocarditis Virus 2A Protein Inhibited Apoptosis by Interaction with Annexin A2 through JNK/c-Jun Pathway.Viruses · 2022Article
- Insights from structural studies of the cardiovirus 2A protein.Bioscience reports · 2022Review
- Structural and molecular basis for Cardiovirus 2A protein as a viral gene expression switch.Nature communications · 2021Article
- Investigating molecular mechanisms of 2A-stimulated ribosomal pausing and frameshifting in Theilovirus.Nucleic acids research · 2021Article
- The location of sensing determines the pancreatic β-cell response to the viral mimetic dsRNA.The Journal of biological chemistry · 2020Article
- A Novel Interaction Network Used by Potyviruses in Virus-Host Interactions at the Protein Level.Viruses · 2019Article
- Characterization of the stimulators of protein-directed ribosomal frameshifting in Theiler's murine encephalomyelitis virus.Nucleic acids research · 2019Article
- Innate Immune Detection of Cardioviruses and Viral Disruption of Interferon Signaling.Frontiers in microbiology · 2018Review
- An analysis by metabolic labelling of the encephalomyocarditis virus ribosomal frameshifting efficiency and stimulators.The Journal of general virology · 2017Article
- Protein-directed ribosomal frameshifting temporally regulates gene expression.Nature communications · 2017Article
- Structures and Corresponding Functions of Five Types of Picornaviral 2A Proteins.Frontiers in microbiology · 2017Review
- Picornaviruses and nuclear functions: targeting a cellular compartment distinct from the replication site of a positive-strand RNA virus.Frontiers in microbiology · 2015Review
- Binding interactions between the encephalomyocarditis virus leader and protein 2A.Journal of virology · 2014Article
- Tinkering with translation: protein synthesis in virus-infected cells.Cold Spring Harbor perspectives in biology · 2013Review
- Cytopathic effects: virus-modulated manifestations of innate immunity?Trends in microbiology · 2012Review
- Host translation at the nexus of infection and immunity.Cell host & microbe · 2012Review
- Site-specific cleavage of the host poly(A) binding protein by the encephalomyocarditis virus 3C proteinase stimulates viral replication.Journal of virology · 2012Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardioviruses have a unique 2A protein (143 aa). During genome translation, the encephalomyocarditis virus (EMCV) 2A is released through a ribosome skipping event mitigated through C-terminal 2A sequences and by subsequent N-terminal reaction with viral 3C(pro). Although viral replication is cytoplasmic, mature 2A accumulates in nucleoli shortly after infection. Some protein also transiently associates with cytoplasmic 40S ribosomal subunits, an activity contributing to inhibition of cellular cap-dependent translation. Cardiovirus sequences predict an eIF4E binding site (aa 126-134) and a nuclear localization signal (NLS, aa 91-102), within 2A, both of which are functional during EMCV infection. Point mutations preventing eIF4E:2A interactions gave small-plaque phenotype viruses, but still inhibited cellular cap-dependent translation. Deletions within the NLS motif relocalized 2A to the cytoplasm and abrogated the inhibition of cap-dependent translation. A fusion protein linking the 2A NLS to eGFP was sufficient to redirect the reporter to the nucleus but not into nucleoli.
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What OpenQuestion holds
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.