| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001541 | Ovarian follicle development | Decreases phenotype | PMID:33197454 |
| GO:0001774 | Microglial cell activation | Increases phenotype | PMID:32522579 |
| GO:0006749 | Glutathione metabolic process | Affects phenotype | PMID:32522579; PMID:32860822 |
| GO:0007253 | Cytoplasmic sequestering of nf-kappab | Decreases phenotype | PMID:22337490 |
| GO:0007283 | Spermatogenesis | Decreases phenotype | PMID:15141104 |
| GO:0007286 | Spermatid development | Affects phenotype | PMID:27466211 |
| GO:0016042 | Lipid catabolic process | Affects phenotype | PMID:32522579; PMID:32860822 |
| GO:0030841 | Positive regulation of intermediate filament polymerization | Increases phenotype | PMID:6361548 |
| GO:0040011 | Locomotion | Affects phenotype | PMID:32522579 |
| GO:0042701 | Progesterone secretion | Affects phenotype | PMID:33197454 |
| GO:0061564 | Axon development | Affects phenotype | PMID:32860822 |
| GO:0061744 | Motor behavior | Affects phenotype | PMID:32522579 |
| GO:0090659 | Walking behavior | Affects phenotype | PMID:31760062; PMID:32860822 |
| GO:1904196 | Negative regulation of granulosa cell proliferation | Increases phenotype | PMID:22337490 |
| GO:1904710 | Positive regulation of granulosa cell apoptotic process | Increases phenotype | PMID:22337490 |
| GO:1905517 | Macrophage migration | Increases phenotype | PMID:32860822 |
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.