ArticleJournal of virology2024
Foot-and-mouth disease virus (FMDV) negatively regulates ZFP36 protein expression to alleviate its antiviral activity.
Article in Journal of virology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed.
- Foot-and-mouth disease virus 3C protease as virulence determinant plays multiple roles in cleaving viral polyprotein and host factors.Virulence · 2026Review
- ZFP36 Family Proteins as Critical Regulators of Inflammation, Immune Cell Development, and Antiviral Responses.Vaccines · 2026Review
- RND3 restricts encephalomyocarditis virus replication by promoting IKKε ubiquitination and type I interferon production.Microbiology spectrum · 2026Article
- Genome-wide CRISPR screen identifies RNF24 as a critical host factor for foot-and-mouth disease virus entry.Frontiers in cell and developmental biology · 2026Article
- Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Zinc finger protein 36 (ZFP36) is a key regulator of inflammatory and cytokine production. However, the interplay between swine zinc-finger protein 36 (sZFP36) and foot-and-mouth disease virus (FMDV) has not yet been reported. Here, we demonstrate that overexpression of sZFP36 restricted FMDV replication, while the knockdown of sZFP36 facilitated FMDV replication. To subvert the antagonism of sZFP36, FMDV decreased sZFP36 protein expression through its non-structural protein 3C protease (3C
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