ArticlePloS one2019
EV71 3C protease induces apoptosis by cleavage of hnRNP A1 to promote apaf-1 translation.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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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
31 citing papers in PubMed, 48 citations in OpenAlex.
- RNF31 restricts EV-A71 replication through innate immune activation and VP4 degradation, and is antagonized by viral 3C proteases.PLoS pathogens · 2026Article
- RasGRP3 Promotes RAP1B Activity to Inhibit Endothelial Inflammation and Alleviate Atherosclerosis in High-Fat Diet-Fed ApoEInflammation · 2026Article
- Virulence determinant of Senecavirus A: 3C protein functions as a protease to cleave viral polyprotein and host factors.Virulence · 2025Review
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Gene Therapy with Enterovirus 3 C Protease: A Promising Strategy for Various Solid Tumors.Nature communications · 2025Article
- HnRNPC triggers the degradation of MITA to suppress the interferon-mediated antiviral response.Veterinary research · 2025Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Decellularized adipose-derived matrix from Superficial layers of abdominal adipose tissue exhibits superior capacity of adipogenesis compared to deep layers.Materials today. Bio · 2024Article
- Enterovirus 3A protein disrupts endoplasmic reticulum homeostasis through interaction with GBF1.Journal of virology · 2024Article
- Readers of RNA Modification in Cancer and Their Anticancer Inhibitors.Biomolecules · 2024Review
- Review
- Picornavirus 3C Proteins Intervene in Host Cell Processes through Proteolysis and Interactions with RNA.Viruses · 2023Review
- Article
- Mechanosensitive extrusion of Enterovirus A71-infected cells from colonic organoids.Nature microbiology · 2023Article
- Gasdermin E is required for induction of pyroptosis and severe disease during enterovirus 71 infection.The Journal of biological chemistry · 2022Article
- The evaluation of both the expression and serum protein levels of Caspase-3 gene in patients with different degrees of SARS-CoV2 infection.Journal of medical virology · 2022Article
- Article
- Multiple functions of heterogeneous nuclear ribonucleoproteins in the positive single-stranded RNA virus life cycle.Frontiers in immunology · 2022Review
- TRAF3IP3 Is Cleaved by EV71 3C Protease and Exhibits Antiviral Activity.Frontiers in microbiology · 2022Article
- Seneca Valley Virus 3CFrontiers in microbiology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Enterovirus 71 (EV71) induces apoptosis to promote viral particle release. Earlier work showed that EV71 utilizes its 3C protease to induce apoptosis in a caspase-3-dependent pathway, though the mechanism is unknown. However, work from Vagner, Holcik and colleagues showed that host protein heterogeneous ribonucleoprotein A1 (hnRNP A1) binds the IRES of cellular apoptotic peptidase activating factor 1 (apaf-1) mRNA to repress its translation. In this work, we show that apaf-1 expression is essential for EV71-induced apoptosis. EV71 infection or ectopic expression of 3C protease cleaves hnRNP A1, which abolishes its binding to the apaf-1 IRES. This allows IRES-dependent synthesis of apaf-1, activation of caspase-3, and apoptosis. Thus, we reveal a novel mechanism that EV71 utilizes for virus release via a 3C protease-hnRNP A1-apaf-1-caspase-3-apoptosis axis.
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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.