ArticlePloS one2013
Enterovirus 71 VP1 activates calmodulin-dependent protein kinase II and results in the rearrangement of vimentin in human astrocyte cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 34 citations in OpenAlex.
- Vimentin Dynamics in Viral Infection: Shield or Sabotage?International journal of molecular sciences · 2025Review
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- Virus-Host Protein Interaction Network of the Hepatitis E Virus ORF2-4 by Mammalian Two-Hybrid Assays.Viruses · 2023Article
- Research progress on pathogenic and therapeutic mechanisms of Enterovirus A71.Archives of virology · 2023Review
- Calpain-2 protein influencesFrontiers in microbiology · 2023Article
- Phosphorylation of ERK-Dependent NF-κB Triggers NLRP3 Inflammasome Mediated by Vimentin in EV71-Infected Glioblastoma Cells.Molecules (Basel, Switzerland) · 2022Article
- Cellular Vimentin Interacts with Foot-and-Mouth Disease Virus Nonstructural Protein 3A and Negatively Modulates Viral Replication.Journal of virology · 2020Article
- Enterovirus A71 capsid protein VP1 increases blood-brain barrier permeability and virus receptor vimentin on the brain endothelial cells.Journal of neurovirology · 2020Article
- Molecular Pathogenicity of Enteroviruses Causing Neurological Disease.Frontiers in microbiology · 2020Review
- Polarized Trout Epithelial Cells Regulate Transepithelial Electrical Resistance, Gene Expression, and the Phosphoproteome in Response to Viral Infection.Frontiers in immunology · 2020Article
- Enterovirus 71 VP1 Protein Regulates Viral Replication in SH-SY5Y Cells via the mTOR Autophagy Signaling Pathway.Viruses · 2019Article
- STAT3 Regulates the Type I IFN-Mediated Antiviral Response by Interfering with the Nuclear Entry of STAT1.International journal of molecular sciences · 2019Article
- Mitochondria Redistribution in Enterovirus A71 Infected Cells and Its Effect on Virus Replication.Virologica Sinica · 2019Article
- Article
- Recent Progress on Functional Genomics Research of Enterovirus 71.Virologica Sinica · 2019Review
- Antiviral and Inflammatory Cellular Signaling Associated with Enterovirus 71 Infection.Viruses · 2018Review
- Enterovirus 71 2B Induces Cell Apoptosis by Directly Inducing the Conformational Activation of the Proapoptotic Protein Bax.Journal of virology · 2016Article
- Phosphoproteomics to Characterize Host Response During Influenza A Virus Infection of Human Macrophages.Molecular & cellular proteomics : MCP · 2016Article
- Bioinformatic analysis of non-VP1 capsid protein of coxsackievirus A6.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2016Article
- Activation of calcium/calmodulin-dependent kinase II following bovine rotavirus enterotoxin NSP4 expression.Iranian journal of basic medical sciences · 2015Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) is one of the main causative agents of foot, hand and mouth disease. Its infection usually causes severe central nervous system diseases and complications in infected infants and young children. In the present study, we demonstrated that EV71 infection caused the rearrangement of vimentin in human astrocytoma cells. The rearranged vimentin, together with various EV71 components, formed aggresomes-like structures in the perinuclear region. Electron microscopy and viral RNA labeling indicated that the aggresomes were virus replication sites since most of the EV71 particles and the newly synthesized viral RNA were concentrated here. Further analysis revealed that the vimentin in the virus factories was serine-82 phosphorylated. More importantly, EV71 VP1 protein is responsible for the activation of calmodulin-dependent protein kinase II (CaMK-II) which phosphorylated the N-terminal domain of vimentin on serine 82. Phosphorylation of vimentin and the formation of aggresomes were required for the replication of EV71 since the latter was decreased markedly after phosphorylation was blocked by KN93, a CaMK-II inhibitor. Thus, as one of the consequences of CaMK-II activation, vimentin phosphorylation and rearrangement may support virus replication by playing a structural role for the formation of the replication factories. Collectively, this study identified the replication centers of EV71 in human astrocyte cells. This may help us understand the replication mechanism and pathogenesis of EV71 in human.
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