ArticleTransboundary and emerging diseases2026
The PCK2-Traf6-Tollip Axis Restricts PEDV Replication by Orchestrating Selective Autophagic Degradation of the Viral Nucleocapsid Protein.
Article in Transboundary and emerging diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- The PCK2-Traf6-Tollip Axis Restricts PEDV Replication by Orchestrating Selective Autophagic Degradation of the Viral Nucleocapsid Protein.Transboundary and emerging diseases · 2026Article
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Authors and funding
11 authors.
Funding
Abstract
Porcine epidemic diarrhea virus (PEDV) is a devastating enteric pathogen in neonatal piglets, causing outbreaks with high mortality. The lack of effective vaccines or treatments makes elucidating host-pathogen interactions essential for developing control strategies. In this study, we identify phosphoenolpyruvate carboxykinase 2 (PCK2) as a host restriction factor that targets the viral nucleocapsid (N) protein for degradation, thereby suppressing PEDV replication. This PCK2-mediated antiviral effect was reversed by autophagy inhibitors, indicating the involvement of a selective autophagic. Mechanistically, we found that PCK2, the N protein, the E3 ubiquitin ligase Traf6, and the cargo receptor Tollip form a functional complex. Depletion of either Traf6 or Tollip disrupted the autophagy pathway, restored N protein stability, and consequently rescued viral replication from PCK2 inhibition. This study unveils a novel antiviral mechanism in which PCK2 orchestrates the selective autophagic degradation of the PEDV N protein, highlighting the PCK2-Traf6-Tollip axis as a promising therapeutic direction.
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