ArticleThe Journal of biological chemistry2011
Sumoylation-promoted enterovirus 71 3C degradation correlates with a reduction in viral replication and cell apoptosis.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 48 citations in OpenAlex.
- Exploring Key Regulators of Mitochondrial Dynamics and Immune Response in SARS-CoV-2 Infection.Viruses · 2026Article
- CBX4 facilitates EV71 replication by SUMOylation and stabilizing 3D polymerase.Frontiers in microbiology · 2026Article
- UBE3C restricts EV-A71 replication by ubiquitination-dependent degradation of 2C.Journal of virology · 2024Article
- AIMP2 restricts EV71 replication by recruiting SMURF2 to promote the degradation of 3D polymerase.Virologica Sinica · 2024Article
- Role of protein Post-translational modifications in enterovirus infection.Frontiers in microbiology · 2024Review
- Mechanosensitive extrusion of Enterovirus A71-infected cells from colonic organoids.Nature microbiology · 2023Article
- Integrated pathway engineering and transcriptome analysis for improved astaxanthin biosynthesis inSynthetic and systems biotechnology · 2022Article
- Multiple-Site SUMOylation of FMDV 3C Protease and Its Negative Role in Viral Replication.Journal of virology · 2022Article
- Enteroviral 2B Interacts with VDAC3 to Regulate Reactive Oxygen Species Generation That Is Essential to Viral Replication.Viruses · 2022Article
- Isolation and Identification of Two Clinical Strains of the Novel GenotypeMicrobiology spectrum · 2022Article
- Neddylation of Enterovirus 71 VP2 Protein Reduces Its Stability and Restricts Viral Replication.Journal of virology · 2022Article
- PIAS1-mediated SUMOylation of influenza A virus PB2 restricts viral replication and virulence.PLoS pathogens · 2022Article
- Coxsackievirus B3 Exploits the Ubiquitin-Proteasome System to Facilitate Viral Replication.Viruses · 2021Article
- Sumoylation of Human Parainfluenza Virus Type 3 Phosphoprotein Correlates with A Reduction in Viral Replication.Virologica Sinica · 2021Article
- Interplay between RNA Viruses and Promyelocytic Leukemia Nuclear Bodies.Veterinary sciences · 2021Review
- Analysis of the Complete Genomes of Enterovirus 71 Subtypes in China.The Canadian journal of infectious diseases & medical microbiology = Journal canadien des maladies infectieuses et de la microbiologie medicale · 2021Article
- Role of Host-Mediated Post-Translational Modifications (PTMs) in RNA Virus Pathogenesis.International journal of molecular sciences · 2020Review
- The Function and Mechanism of Enterovirus 71 (EV71) 3C Protease.Current microbiology · 2020Review
- Article
- SUMO and Cytoplasmic RNA Viruses: From Enemies to Best Friends.Advances in experimental medicine and biology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71), a member of the Picornaviridae family, may cause serious clinical manifestations associated with the central nervous system. Enterovirus 3C protease is required for virus replication and can trigger host cell apoptosis via cleaving viral polyprotein precursor and cellular proteins, respectively. Although the role of the 3C protease in processing viral and cellular proteins has been established, very little is known about the modulation of EV71 3C function by host cellular factors. Here, we show that sumoylation promotes EV71 3C protein ubiquitination for degradation, correlating with a decrease of EV71 in virus replication and cell apoptosis. SUMO E2-conjugating enzyme Ubc9 was identified as an EV71 3C-interacting protein. Further studies revealed that EV71 3C can be SUMO (small ubiquitin-like modifier)-modified at residue Lys-52. Sumoylation down-regulated 3C protease activity in vitro and also 3C protein stability in cells, in agreement with data suggesting 3C K52R protein induced greater substrate cleavage and apoptosis in cells. More importantly, the recombinant EV71 3C K52R virus infection conferred more apoptotic phenotype and increased virus levels in culture cells, which also correlated with a mouse model showing increased levels of viral VP1 protein in intestine and neuron loss in the spinal cord with EV71 3C K52R recombinant viral infection. Finally, we show that EV71 3C amino acid residues 45-52 involved in Ubc9 interaction determined the extent of 3C sumoylation and protein stability. Our results uncover a previously undescribed cellular regulatory event against EV71 virus replication and host cell apoptosis by sumoylation at 3C protease.
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