| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001541 | Ovarian follicle development | Affects phenotype | PMID:34383603 |
| GO:0001547 | Antral ovarian follicle growth | Affects phenotype | PMID:34383603 |
| GO:0001552 | Ovarian follicle atresia | Affects phenotype | PMID:34383603 |
| GO:0007281 | Germ cell development | Affects phenotype | PMID:34383603 |
| GO:0033148 | Positive regulation of intracellular estrogen receptor signaling pathway | Increases phenotype | PMID:25449125 |
| GO:0035064 | Methylated histone binding | Affects phenotype | PMID:34383603 |
| GO:0042711 | Maternal behavior | Affects phenotype | PMID:34383603 |
| GO:0043970 | Histone h3-k9 acetylation | Affects phenotype | PMID:34383603 |
| GO:0044849 | Estrous cycle | Affects phenotype | PMID:34383603 |
| GO:0048135 | Female germ-line cyst formation | Affects phenotype | PMID:34383603 |
| GO:0060207 | Diestrus | Affects phenotype | PMID:34383603 |
| GO:0060208 | Proestrus | Affects phenotype | PMID:34383603 |
| GO:0060209 | Estrus | Affects phenotype | PMID:34383603 |
| GO:0061628 | H3k27me3 modified histone binding | Affects phenotype | PMID:34383603 |
| GO:0070577 | Lysine-acetylated histone binding | Affects phenotype | PMID:34383603 |
| GO:0080182 | Histone h3-k4 trimethylation | Affects phenotype | PMID:34383603 |
| GO:0098532 | Histone h3-k27 trimethylation | Affects phenotype | PMID:34383603 |
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.