ArticleVirus research2024
ZFP36 Facilitates Senecavirus A (SVA) replication by inhibiting the production of type I interferon.
Article in Virus research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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
3 citing papers in PubMed.
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Zinc finger proteins (ZFPs) play an important role in the host-virus interplay. Zinc finger protein 36 is a member of the zinc finger protein 36 family, which includes two other paralogs, namely ZFP36L1 and ZFP36L2. Studies have demonstrated that ZFP36L1 acts as a host defender against influenza A virus and flaviviruses. However, the role of ZFP36 in host-virus interactions has not been thoroughly investigated. Here, we demonstrated that human zinc finger protein 36 (hZFP36) exhibited potent pro-viral activity during Senecavirus A infection. Overexpression of ZFP36 facilitated Senecavirus A infection, while hZFP36 knockdown inhibited viral replication. The ZF motifs of hZFP36 are key for promoting viral proliferation. hZFP36 stabilized Senecavirus A VP1 by binding to it. Furthermore, hZFP36 inhibited SeV-mediated IFN-β production through inducing caspase-dependent cleavage for MAVS. These findings provide insights into the mechanism of action of ZFP36 in host-virus interactions.
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