| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001662 | Behavioral fear response | Affects phenotype | PMID:23260230 |
| GO:0001820 | Serotonin secretion | Increases phenotype | PMID:30592962 |
| GO:0006309 | Apoptotic dna fragmentation | Increases phenotype | PMID:9669204 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:10487422; PMID:8722508; PMID:9443068; PMID:9669204 |
| GO:0006929 | Substrate-dependent cell migration | Increases phenotype | PMID:30592962 |
| GO:0006979 | Response to oxidative stress | Increases phenotype | PMID:10487422 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:25038229 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:28467792 |
| GO:0036276 | Response to antidepressant | Increases phenotype | PMID:29107002 |
| GO:0042427 | Serotonin biosynthetic process | Decreases phenotype | PMID:28263910 |
| GO:0046460 | Neutral lipid biosynthetic process | Increases phenotype | PMID:38643950 |
| GO:0046847 | Filopodium assembly | Increases phenotype | PMID:30592962 |
| GO:0070527 | Platelet aggregation | Increases phenotype | PMID:30592962 |
| GO:1905673 | Positive regulation of lysosome organization | Increases phenotype | PMID:38643950 |
| GO:2000845 | Positive regulation of testosterone secretion | Decreases phenotype | PMID:26162595 |
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.