Flusilazole


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001843 Neural tube closure Decreases phenotype PMID:28263823
GO:0002072 Optic cup morphogenesis involved in camera-type eye development Decreases phenotype PMID:28263823
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:32810590; PMID:34273450; PMID:34273450
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:34537371; PMID:34737147
GO:0009410 Response to xenobiotic stimulus Increases phenotype PMID:34537371
GO:0010942 Positive regulation of cell death Increases phenotype PMID:40434365
GO:0042307 Positive regulation of protein import into nucleus Decreases phenotype PMID:24154490
GO:0045444 Fat cell differentiation Increases phenotype PMID:32473317
GO:0048863 Stem cell differentiation Decreases phenotype PMID:32205227
GO:0050810 Regulation of steroid biosynthetic process Affects phenotype PMID:26781511
GO:0055007 Cardiac muscle cell differentiation Decreases phenotype PMID:24704097; PMID:29337257
GO:0060037 Pharyngeal system development Decreases phenotype PMID:28263823
GO:0106135 Negative regulation of cardiac muscle cell contraction Increases phenotype PMID:34737147
GO:2000726 Negative regulation of cardiac muscle cell differentiation Increases phenotype PMID:34537371; PMID:34737147

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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.