ArticleFrontiers in microbiology2019
Elucidating the Host Interactome of EV-A71 2C Reveals Viral Dependency Factors.
Article in Frontiers in microbiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- The neddylation of the RNA-dependent RNA polymerase 3D of Coxsackievirus B3 promotes viral replication.Journal of virology · 2025Article
- ARFGAP1 serves as a critical host factor during E30 infection: QS11 inhibits viral pathogenesis in hFcRn-IFNARVirology journal · 2025Article
- Review
- UBE3C restricts EV-A71 replication by ubiquitination-dependent degradation of 2C.Journal of virology · 2024Article
- Advances in anti-EV-A71 drug development research.Journal of advanced research · 2024Review
- Picornavirus 2C proteins: structure-function relationships and interactions with host factors.Frontiers in cellular and infection microbiology · 2024Review
- The Structure, Function, and Mechanisms of Action of Enterovirus Non-structural Protein 2C.Frontiers in microbiology · 2020Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Viral protein 2C plays a critical role in EV-A71 replication. The discovery of 2C binding proteins will likely provide potential targets to treat EV-A71 infection. Here, we provide a global proteomic analysis of the human proteins that interact with the EV-A71 2C protein. TRIM4, exportin2, and ARFGAP1 were validated as 2C binding partners. Further functional studies revealed that TRIM4, exportin2, and ARFGAP1 were novel host dependency factors for EV-A71. Moreover, enteroviruses' 2C family proteins interacted with exportin2 and ARFGAP1. In conclusion, our study provides a cellular interactome of the EV-A71 2C and identifies the proviral roles of TRIM4, exportin2, and ARFGAP1 in EV-A71 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.