Equol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001503 Ossification Decreases phenotype PMID:39743035
GO:0001552 Ovarian follicle atresia Increases phenotype PMID:26876617
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:35986755
GO:0006749 Glutathione metabolic process Affects phenotype PMID:39743035
GO:0006811 Monoatomic ion transport Increases phenotype PMID:18651719
GO:0008209 Androgen metabolic process Affects phenotype PMID:26876617
GO:0008210 Estrogen metabolic process Affects phenotype PMID:26876617
GO:0008283 Cell population proliferation Increases phenotype PMID:39743035
GO:0030036 Actin cytoskeleton organization Affects phenotype PMID:32963737
GO:0031941 Filamentous actin Affects phenotype PMID:32963737
GO:0042448 Progesterone metabolic process Affects phenotype PMID:26876617
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:26876617
GO:0044237 Cellular metabolic process Affects phenotype PMID:35986755
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:39743035
GO:2000388 Positive regulation of antral ovarian follicle growth Decreases phenotype PMID:26876617
DISCLAIMER

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.