ArticleVeterinary sciences2025
4D-DIA Proteomic Analysis of IPEC-J2 Cells Infected with Porcine Group A Rotavirus G9P[23] Strain.
Article in Veterinary sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Establishment of a Porcine Small Intestinal Organoid Model for Porcine Rotavirus Infection.Animals : an open access journal from MDPI · 2026Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Porcine rotavirus (PoRV) is one of the most devastating enteric pathogens causing gastroenteritis in pigs, particularly the sudden occurrence in recent years in China. To elucidate host-pathogen interactions and molecular mechanisms underlying PoRV pathogenesis, four-dimensional (4D) data-independent acquisition (DIA) proteomic (4D-DIA) analysis was performed to comprehensively quantify the differentially abundant proteins (DAPs) in PoRV-infected IPEC-J2 cells. A total of 8725 cellular proteins were identified with 279 more abundant and 356 down abundant proteins. A Western blot showed that the abundance of SA100A8, DAPK2, and FTL were in accordance with the acquired proteomic data using 4D-DIA analysis. Bioinformatics analyses of GO and KEGG demonstrated that various DAPs are involved in crucial biological processes and signaling pathways, such as immune response, signal transduction, metabolic pathways, autophagy, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction. Notably, inflammatory features of host response upon PoRV infection were highlighted, with RT-qPCR confirming the significant upregulation of IL-1α, IL-6, IL-8, TNF-α, STAT1, and IRF9 transcript levels during infection. Altogether, our preliminary findings advance our understanding of PoRV pathogenesis and may shed light on identifying potential targets for the prevention and control of PoRV-associated gastroenteritis.
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