ArticleToxins2016
Phosphoproteome Analysis Reveals the Molecular Mechanisms Underlying Deoxynivalenol-Induced Intestinal Toxicity in IPEC-J2 Cells.
Article in Toxins, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 28 citations in OpenAlex.
- Deoxynivalenol-induced cellular signal transduction: research progress on toxicological effects, molecular mechanisms, and biological intervention strategies.Molecular biology reports · 2026Review
- Mycotoxin-Caused Intestinal Toxicity: Underlying Molecular Mechanisms and Further Directions.Toxics · 2025Review
- Protective effects of bone marrow mesenchymal stem cell-derived exosomes loaded cerium dioxide nanoparticle against deoxynivalenol-induced liver damage.Journal of nanobiotechnology · 2025Article
- Selenomethionine Alleviates Deoxynivalenol-Induced Oxidative Injury in Porcine Intestinal Epithelial Cells Independent of MAPK Pathway Regulation.Antioxidants (Basel, Switzerland) · 2024Article
- Determination ofFrontiers in toxicology · 2024Article
- MicroRNA Expression Profiling in Porcine Liver, Jejunum and Serum upon Dietary DON Exposure Reveals Candidate Toxicity Biomarkers.International journal of molecular sciences · 2021Article
- Deoxynivalenol and Zearalenone-Synergistic or Antagonistic Agri-Food Chain Co-Contaminants?Toxins · 2021Review
- Article
- Deoxynivalenol Induces Inflammation in the Small Intestine of Weaned Rabbits by Activating Mitogen-Activated Protein Kinase Signaling.Frontiers in veterinary science · 2021Article
- Deoxynivalenol Induces Inflammation in IPEC-J2 Cells by Activating P38 Mapk And Erk1/2.Toxins · 2020Article
- Comparative Transcriptome Analysis Reveals the Protective Mechanism of Glycyrrhinic Acid for Deoxynivalenol-Induced Inflammation and Apoptosis in IPEC-J2 Cells.Oxidative medicine and cellular longevity · 2020Article
- Deoxynivalenol Induces Inflammatory Injury in IPEC-J2 Cells via NF-κB Signaling Pathway.Toxins · 2019Article
- Article
- Effects of Saccharomyces cerevisiae on alleviating cytotoxicity of porcine jejunal epithelia cells induced by deoxynivalenol.AMB Express · 2019Article
- Article
- Deoxynivalenol Modulates the Viability, ROS Production and Apoptosis in Prostate Cancer Cells.Toxins · 2019Article
- Effects of deoxynivalenol- and zearalenone-contaminated feed on the gene expression profiles in the kidneys of piglets.Asian-Australasian journal of animal sciences · 2018Article
- Forthcoming Challenges in Mycotoxins Toxicology Research for Safer Food-A Need for Multi-Omics Approach.Toxins · 2017Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Deoxynivalenol (DON) is a widespread trichothecene mycotoxin that commonly contaminates cereal crops and has various toxic effects in animals and humans. DON primarily targets the gastrointestinal tract, the first barrier against ingested food contaminants. In this study, an isobaric tag for relative and absolute quantitation (iTRAQ)-based phosphoproteomic approach was employed to elucidate the molecular mechanisms underlying DON-mediated intestinal toxicity in porcine epithelial cells (IPEC-J2) exposed to 20 μM DON for 60 min. There were 4153 unique phosphopeptides, representing 389 phosphorylation sites, detected in 1821 phosphoproteins. We found that 289 phosphopeptides corresponding to 255 phosphoproteins were differentially phosphorylated in response to DON. Comprehensive Gene Ontology (GO) analysis combined with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment revealed that, in addition to previously well-characterized mitogen-activated protein kinase (MAPK) signaling, DON exposure altered phosphatidylinositol 3-kinase/Akt (PI3K/Akt) and Janus kinase/signal transducer, and activator of transcription (JAK/STAT) pathways. These pathways are involved in a wide range of biological processes, including apoptosis, the intestinal barrier, intestinal inflammation, and the intestinal absorption of glucose. DON-induced changes are likely to contribute to the intestinal dysfunction. Overall, identification of relevant signaling pathways yielded new insights into the molecular mechanisms underlying DON-induced intestinal toxicity, and might help in the development of improved mechanism-based risk assessments in animals and humans.
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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.