ArticleProceedings of the National Academy of Sciences of the United States of America1996
Activation of the translational suppressor 4E-BP1 following infection with encephalomyocarditis virus and poliovirus.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.
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Who cites it
105 citing papers in PubMed, 233 citations in OpenAlex.
- SIRT2 mediates integrated stress response by deacetylating and stabilizing 4E-BP1 to suppress translation.EMBO reports · 2026Article
- Eukaryotic translation initiation factor 4F: functional properties and physiological role.Nucleic acids research · 2025Review
- The p48 isoform of the PA2G4/EBP1/ITAF45 oncoprotein is required for the encephalomyocarditis virus IRES-driven translation initiation.Nucleic acids research · 2025Article
- Translation of nervous necrosis virus involves eIF4E but not RPS6 phosphorylation and viral particle assembly in remodeled microtubule-organizing center.Virology journal · 2025Article
- Polyglutamine-mediated ribotoxicity disrupts proteostasis and stress responses in Huntington's disease.Nature cell biology · 2024Article
- Host-like RNA Elements Regulate Virus Translation.Viruses · 2024Review
- Coronavirus takeover of host cell translation and intracellular antiviral response: a molecular perspective.The EMBO journal · 2024Review
- 4E-BP1-dependent translation in nociceptors controls mechanical hypersensitivity via TRIM32/type I interferon signaling.Science advances · 2023Article
- Arabidopsis eIF4E1 protects the translational machinery during TuMV infection and restricts virus accumulation.PLoS pathogens · 2023Article
- Picornavirus translation strategies.FEBS open bio · 2022Review
- PABP1 Drives the Selective Translation of Influenza A Virus mRNA.Journal of molecular biology · 2022Article
- Minding the message: tactics controlling RNA decay, modification, and translation in virus-infected cells.Genes & development · 2022Review
- Insights from structural studies of the cardiovirus 2A protein.Bioscience reports · 2022Review
- Review
- Ribosomal control in RNA virus-infected cells.Frontiers in microbiology · 2022Review
- Article
- Non-Canonical Translation Initiation Mechanisms Employed by Eukaryotic Viral mRNAs.Biochemistry. Biokhimiia · 2021Review
- RNA-Binding Proteins at the Host-Pathogen Interface Targeting Viral Regulatory Elements.Viruses · 2021Article
- Roadblocks and fast tracks: How RNA binding proteins affect the viral RNA journey in the cell.Seminars in cell & developmental biology · 2021Review
- Duck Hepatitis A Virus Type 1 Induces eIF2α Phosphorylation-Dependent Cellular Translation ShutoffFrontiers in microbiology · 2021Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Infection of cells with picornaviruses, such as poliovirus and encephalomyocarditis virus (EMCV), causes a shutoff of host protein synthesis. The molecular mechanism of the shutoff has been partly elucidated for poliovirus but not for EMCV. Translation initiation in eukaryotes is facilitated by the mRNA 5' cap structure to which the multisubunit translation initiation factor eIF4F binds to promote ribosome binding. Picornaviruses use a mechanism for the translation of their RNA that is independent of the cap structure. Poliovirus infection engenders the cleavage of the eIF4G (formerly p220) component of eIF4F and renders this complex inactive for cap-dependent translation. In contrast, EMCV infection does not result in eIF4G cleavage. Here, we report that both EMCV and poliovirus activate a translational repressor, 4E-BP1, that inhibits cap-dependent translation by binding to the cap-binding subunit eIF4E. Binding of eIF4E occurs only to the underphosphorylated form of 4E-BP1, and this interaction is highly regulated in cells. We show that 4E-BP1 becomes dephosphorylated upon infection with both EMCV and poliovirus. Dephosphorylation of 4E-BP1 temporally coincides with the shutoff of protein synthesis by EMCV but lags behind the shutoff and eIF4G cleavage in poliovirus-infected cells. Dephosphorylation of 4E-BP1 by specifically inhibiting cap-dependent translation may be the major cause of the shutoff phenomenon in EMCV-infected cells.
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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.