ArticleCell cycle (Georgetown, Tex.)2015
Enterovirus 71 mediates cell cycle arrest in S phase through non-structural protein 3D.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 54 citations in OpenAlex.
- Genistein inhibits the replication of enterovirus A71.Frontiers in pharmacology · 2026Article
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Genotoxic consequences of viral infections.Npj viruses · 2025Review
- GRP78 recognizes EV-F 3D protein and activates NF-κB to repress virus replication by interacting with CHUK/IKBKB.Journal of virology · 2024Article
- Multiple functions of the nonstructural protein 3D in picornavirus infection.Frontiers in immunology · 2024Review
- Regulation of host factor γ-H2AX level and location by enterovirus A71 for viral replication.Virulence · 2022Article
- Duck hepatitis A virus type 1 mediates cell cycle arrest in the S phase.Virology journal · 2022Article
- Fucosylated oligosaccharide Lacto-Food chemistry: X · 2022Article
- The C/EBPβ-Dependent Induction of TFDP2 Facilitates Porcine Reproductive and Respiratory Syndrome Virus Proliferation.Virologica Sinica · 2021Article
- Multiple RNA virus matrix proteins interact with SLD5 to manipulate host cell cycle.The Journal of general virology · 2021Article
- Circ_RPL23A acts as a miR-1233 sponge to suppress the progression of clear cell renal cell carcinoma by promoting ACAT2.Journal of bioenergetics and biomembranes · 2021Article
- PRRSV Promotes MARC-145 Cells Entry Into S Phase of the Cell Cycle to Facilitate Viral ReplicationFrontiers in veterinary science · 2021Article
- Enterovirus 71 induces neural cell apoptosis and autophagy through promoting ACOX1 downregulation and ROS generation.Virulence · 2020Article
- Transcriptome analysis following enterovirus 71 and coxsackievirus A16 infection in respiratory epithelial cells.Archives of virology · 2020Article
- Caspase-3 inhibitor inhibits enterovirus D68 production.Journal of microbiology (Seoul, Korea) · 2020Article
- Article
- miR-431 regulates granulosa cell function through the IRS2/PI3K/AKT signaling pathway.The Journal of reproduction and development · 2020Article
- Alphaherpesvirus Major Tegument Protein VP22: Its Precise Function in the Viral Life Cycle.Frontiers in microbiology · 2020Review
- Enterovirus and Encephalitis.Frontiers in microbiology · 2020Review
- Association of IGF1R polymorphisms (rs1546713) with susceptibility to age-related cataract in a Han Chinese population.International journal of ophthalmology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 3 countries.
Funding
Abstract
Many viruses disrupt the host cell cycle to facilitate their own growth. We assessed the mechanism and function of enterovirus 71 (EV71), a primary causative agent for recent hand, foot, and mouth disease outbreaks, in manipulating cell cycle progression. Our results suggest that EV71 infection induces S-phase arrest in diverse cell types by preventing the cell cycle transition from the S phase into the G2/M phase. Similar results were observed for an alternate picornavirus, Coxsackievirus A16. Synchronization in S phase, but not G0/G1 phase or G2/M phase, promotes viral replication. Consistent with its ability to arrest cells in S phase, the expression of cyclin A2, CDK 2, cyclin E1, and cyclin B1 was regulated by EV71 through increasing transcription of cyclin E1, promoting proteasome-mediated degradation of cyclin A2 and regulating the phosphorylation of CDK 2. Finally, a non-structural protein of EV71, the RNA-dependent RNA polymerase 3D, was demonstrated to mediate S-phase cell cycle arrest. These findings suggest that EV71 induces S-phase cell cycle arrest in infected cells via non-structural protein 3D, which may provide favorable conditions for virus production.
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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.