| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0006304 | Dna modification | Decreases phenotype | PMID:28659405 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:15820723 |
| GO:0006979 | Response to oxidative stress | Increases phenotype | PMID:15820723 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:23913582 |
| GO:0016477 | Cell migration | Affects phenotype | PMID:23913582 |
| GO:0033148 | Positive regulation of intracellular estrogen receptor signaling pathway | Increases phenotype | PMID:26022396 |
| GO:0033993 | Response to lipid | Decreases phenotype | PMID:28659405 |
| GO:0043433 | Negative regulation of dna-binding transcription factor activity | Increases phenotype | PMID:26022396 |
| GO:0050679 | Positive regulation of epithelial cell proliferation | Decreases phenotype | PMID:28659405 |
| GO:0050847 | Progesterone receptor signaling pathway | Decreases phenotype | PMID:26022396 |
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.