ArticleViruses2020
Beclin1 Binds to Enterovirus 71 3D Protein to Promote the Virus Replication.
Article in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 17 citations in OpenAlex.
- Picornavirus VP2 protein suppresses innate immunity through selective autophagic degradation of IKBKE/IKKε.Autophagy · 2026Article
- Porcine Beclin1 facilitates the proliferation of porcine circovirus type 2 by augmenting autophagy in PK-15 cells.Frontiers in cellular and infection microbiology · 2026Article
- Lipoprotein (a) fuels EV71 replication by activating p38 MAPK-autophagy axis.Frontiers in immunology · 2026Article
- A Focus on Natural Autophagy Modulators as Potential Host-Directed Weapons Against Emerging and Re-Emerging Viruses.Medicinal research reviews · 2025Review
- Article
- Hijacking the Host Cell for Replication: Pro-Viral Host Factors Involved in EVA71 Infection.International journal of molecular sciences · 2025Review
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- The multiple roles of viral 3DVirulence · 2024Review
- 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
- Autophagy and Inflammation: Regulatory Roles in Viral Infections.Biomolecules · 2023Review
- In Memory of the Virologist Jianguo Wu, 1957-2022.Viruses · 2023Article
- TRAF3 activates STING-mediated suppression of EV-A71 and target of viral evasion.Signal transduction and targeted therapy · 2023Article
- Dysregulated autophagy contributes to the pathogenesis of enterovirus A71 infection.Cell & bioscience · 2020Review
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 the main pathogen causing hand-foot-mouth disease (HFMD) in infants and children, which can also lead to severe neurological diseases and even death. Therefore, understanding the replication mechanism of EV71 is of great significance for the prevention and control of EV71-induced diseases. Beclin1 (BECN1, a mammalian homologue of ATG6 in yeast) is an important core protein for the initiation and the normal process of autophagy in cells. In addition to its involvement in autophagy, Beclin1 has also been reported to play an important role in cancer and innate immune signaling pathways. However, the role of Beclin1 in EV71 replication remains elusive. Here, we primarily found that Beclin1 facilitates EV71 replication in human rhabdomyosarcoma (RD) cells and the autophagy was actually induced, but Beclin1 was not significantly affected at either mRNA level or protein level during early EV71 infection. Further studies discovered that Beclin1 could interacts with EV71 non-structural protein 3D mainly through its evolutionary conserved domain (ECD) and coiled-coiled domain (CCD), thus promoting the replication of EV71 in human rhabdomyosarcoma (RD) cells and human astroglioma (U251) cells. Collectively, we reveal a novel regulatory mechanism associated with Beclin1 to promote EV71 replication, thus providing a potential therapeutic target for the prevention and control of EV71-associated diseases.
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