| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0004035 | Alkaline phosphatase activity | Increases phenotype | PMID:35986755 |
| GO:0006874 | Cellular calcium ion homeostasis | Affects phenotype | PMID:27224899; PMID:33689779 |
| GO:0010940 | Positive regulation of necrotic cell death | Increases phenotype | PMID:35163327 |
| GO:0030879 | Mammary gland development | Affects phenotype | PMID:35163327 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:30610963; PMID:35986755 |
| GO:0070374 | Positive regulation of erk1 and erk2 cascade | Affects phenotype | PMID:23538034 |
| GO:0070509 | Calcium ion import | Increases phenotype | PMID:33689779 |
| GO:0090037 | Positive regulation of protein kinase c signaling | Affects phenotype | PMID:23538034 |
| GO:2000865 | Negative regulation of estradiol secretion | Increases phenotype | PMID:35163327 |
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.