Fludioxonil


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:34503147
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:33575850
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:19591892
GO:0008283 Cell population proliferation Affects phenotype PMID:28855101; PMID:34503147
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:27539251
GO:0010718 Positive regulation of epithelial to mesenchymal transition Increases phenotype PMID:27539251
GO:0030335 Positive regulation of cell migration Increases phenotype PMID:27539251
GO:0031393 Negative regulation of prostaglandin biosynthetic process Increases phenotype PMID:26359731
GO:0034109 Homotypic cell-cell adhesion Increases phenotype PMID:34503147
GO:0036164 Cell-abiotic substrate adhesion Decreases phenotype PMID:34503147
GO:0045333 Cellular respiration Increases phenotype PMID:34503147
GO:0046034 Atp metabolic process Affects phenotype PMID:34503147
GO:0048870 Cell motility Increases phenotype PMID:34503147
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We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.