ArticleJournal of virology2017
Enterovirus 71 3C Promotes Apoptosis through Cleavage of PinX1, a Telomere Binding Protein.
Article in Journal of virology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Cleavage of Stau2 by 3C protease promotes EV-A71 replication.Virology journal · 2024Article
- Picornavirus VP3 protein induces autophagy through the TP53-BAD-BAX axis to promote viral replication.Autophagy · 2024Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- TRAF3IP3 Is Cleaved by EV71 3C Protease and Exhibits Antiviral Activity.Frontiers in microbiology · 2022Article
- 3C protease of enterovirus 71 cleaves promyelocytic leukemia protein and impairs PML-NBs production.Virology journal · 2021Article
- Ectopic Expression of TRIM25 Restores RIG-I Expression and IFN Production Reduced by Multiple Enteroviruses 3CVirologica Sinica · 2021Article
- Embryotoxic activity of 3C protease of human hepatitis A virus in developing Danio rerio embryos.Scientific reports · 2021Article
- Intrinsic apoptosis and cytokine induction regulated in human tonsillar epithelial cells infected with enterovirus A71.PloS one · 2021Article
- SARS-CoV-2 Membrane Glycoprotein M Triggers Apoptosis With the Assistance of Nucleocapsid Protein N in Cells.Frontiers in cellular and infection microbiology · 2021Article
- Heat Shock Protein A6, a Novel HSP70, Is Induced During Enterovirus A71 Infection to Facilitate Internal Ribosomal Entry Site-Mediated Translation.Frontiers in microbiology · 2021Article
- Enterovirus 71 induces neural cell apoptosis and autophagy through promoting ACOX1 downregulation and ROS generation.Virulence · 2020Article
- Recent advances of enterovirus 71Virology journal · 2020Review
- Can charcoal improve outcomes in COVID-19 infections?Medical hypotheses · 2020Article
- The Function and Mechanism of Enterovirus 71 (EV71) 3C Protease.Current microbiology · 2020Review
- The Heat Shock Protein 70 Family of Chaperones Regulates All Phases of the Enterovirus A71 Life Cycle.Frontiers in microbiology · 2020Article
- Regulation of Apoptosis by Enteroviruses.Frontiers in microbiology · 2020Review
- Activity-Based Protein Profiling Identifies ATG4B as a Key Host Factor for Enterovirus 71 Proliferation.Journal of virology · 2019Article
- STAT3 Regulates the Type I IFN-Mediated Antiviral Response by Interfering with the Nuclear Entry of STAT1.International journal of molecular sciences · 2019Article
- Recent Progress on Functional Genomics Research of Enterovirus 71.Virologica Sinica · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is an emerging pathogen causing hand, foot, and mouth disease (HFMD) and fatal neurological diseases in infants and young children due to their underdeveloped immunocompetence. EV71 infection can induce cellular apoptosis through a variety of pathways, which promotes EV71 release. The viral protease 3C plays an important role in EV71-induced apoptosis. However, the molecular mechanism responsible for 3C-triggered apoptosis remains elusive. Here, we found that EV71 3C directly interacted with PinX1, a telomere binding protein. Furthermore, 3C cleaved PinX1 at the site of Q50-G51 pair through its protease activity. Overexpression of PinX1 reduced the level of EV71-induced apoptosis and EV71 release, whereas depletion of PinX1 by small interfering RNA promoted apoptosis induced by etoposide and increased EV71 release. Taken together, our study uncovered a mechanism that EV71 utilizes to promote host cell apoptosis through cleavage of cellular protein PinX1 by 3C. IMPORTANCE: EV71 3C plays an important role in processing viral proteins and interacting with host cells. In this study, we showed that 3C promoted apoptosis through cleaving PinX1, a telomere binding protein, and that this cleavage facilitated EV71 release. Our study demonstrated that PinX1 plays an important role in EV71 release and revealed a novel mechanism that EV71 utilizes to induce apoptosis. This finding is important in understanding EV71-host cell interactions and has potential impact on understanding other enterovirus-host cell interactions.
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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.