| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0006304 | Dna modification | Increases phenotype | PMID:26377693 |
| GO:0006749 | Glutathione metabolic process | Increases phenotype | PMID:29526570 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:29526570 |
| GO:0042593 | Glucose homeostasis | Affects phenotype | PMID:37019984 |
| GO:1900119 | Positive regulation of execution phase of apoptosis | Increases phenotype | PMID:29526570 |
| GO:1901670 | Negative regulation of superoxide dismutase activity | Increases phenotype | PMID:29526570 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:29526570 |
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.