ArticleVirology2016
ATP1B3: a virus-induced host factor against EV71 replication by up-regulating the production of type-I interferons.
Article in Virology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Insight into the Life Cycle of Enterovirus-A71.Viruses · 2025Review
- Interaction Network Characterization of Infectious Bronchitis Virus Nsp2 with Host Proteins.Veterinary sciences · 2024Article
- Current status of hand-foot-and-mouth disease.Journal of biomedical science · 2023Review
- Hand-Foot-and-Mouth Disease-Associated Enterovirus and the Development of Multivalent HFMD Vaccines.International journal of molecular sciences · 2022Review
- ATP5B Is an Essential Factor for Hepatitis B Virus Entry.International journal of molecular sciences · 2022Article
- Covid-19 and development of heart failure: mystery and truth.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
- Picornaviruses: A View from 3A.Viruses · 2021Review
- DEAD-Box Helicase DDX6 Facilitated RIG-I-Mediated Type-I Interferon Response to EV71 Infection.Frontiers in cellular and infection microbiology · 2021Article
- ATP1B3 cooperates with BST-2 to promote hepatitis B virus restriction.Journal of medical virology · 2020Article
- Interplay between FACT subunit SPT16 and TRIM33 can remodel chromatin at macrophage distal regulatory elements.Epigenetics & chromatin · 2019Article
- The Antiviral Effects of Na,K-ATPase Inhibition: A Minireview.International journal of molecular sciences · 2018Review
- Enterovirus A71 Proteins: Structure and Function.Frontiers in microbiology · 2018Review
- Expression of the β3 subunit of NaOncotarget · 2017Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Enterovirus 71 (EV71) infection can cause severe diseases, and is becoming increasingly common in children. In the current study, we carried out yeast two-hybrid assays to screen human proteins that could interact with 3A protein of EV71. Human β3 subunit of Na(+)/K(+)-ATPase (ATP1B3) protein was demonstrated to interact with the 3A protein of EV71. Although 3A protein had no effect on the expression of ATP1B3, EV71 infection resulted in elevated expression of ATP1B3 in RD cell line, both on messenger RNA (mRNA) and protein levels. Interestingly, knockdown of ATP1B3 could significantly increase the replication of EV71, whereas overexpression of ATP1B3 significantly suppressed the replication of EV71 in RD cells. Furthermore, we demonstrated that the expression of ATP1B3 could induce the production of type-I interferons. Our study demonstrated that ATP1B3 inhibit EV71 replication by enhancing the production of type-I interferons, which could act as a potential therapeutic target in EV71 infection.
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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.