| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0004784 | Superoxide dismutase activity | Increases phenotype | PMID:39197506 |
| GO:0006506 | Gpi anchor biosynthetic process | Decreases phenotype | PMID:27931811 |
| GO:0006749 | Glutathione metabolic process | Affects phenotype | PMID:39197506 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:10753191; PMID:24594278; PMID:28688903 |
| GO:0006974 | Cellular response to dna damage stimulus | Affects phenotype | PMID:27059372; PMID:27233451 |
| GO:0008210 | Estrogen metabolic process | Affects phenotype | PMID:39197506 |
| GO:0008219 | Cell death | Increases phenotype | PMID:30336191 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:24594278; PMID:35598691; PMID:38977090 |
| GO:0022008 | Neurogenesis | Affects phenotype | PMID:24463056 |
| GO:0032125 | Micronucleus organization | Increases phenotype | PMID:29110037; PMID:30944280 |
| GO:0034440 | Lipid oxidation | Affects phenotype | PMID:39197506 |
| GO:0042221 | Response to chemical | Increases phenotype | PMID:34428494 |
| GO:0042448 | Progesterone metabolic process | Affects phenotype | PMID:39197506 |
| GO:0042756 | Drinking behavior | Affects phenotype | PMID:38977090 |
| GO:0043967 | Histone h4 acetylation | Decreases phenotype | PMID:27233451 |
| GO:0043981 | Histone h4-k5 acetylation | Decreases phenotype | PMID:27233451 |
| GO:0043982 | Histone h4-k8 acetylation | Decreases phenotype | PMID:27233451 |
| GO:0043983 | Histone h4-k12 acetylation | Decreases phenotype | PMID:27233451 |
| GO:0045930 | Negative regulation of mitotic cell cycle | Increases phenotype | PMID:29110037 |
| GO:0046209 | Nitric oxide metabolic process | Affects phenotype | PMID:39197506 |
| GO:2000252 | Negative regulation of feeding behavior | Increases phenotype | PMID:38977090 |
| GO:2000279 | Negative regulation of dna biosynthetic process | Decreases phenotype | PMID:2909289 |
| GO:2000619 | Negative regulation of histone h4-k16 acetylation | Increases phenotype | PMID:27233451 |
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.