| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0002523 | Leukocyte migration involved in inflammatory response | Increases phenotype | PMID:37598415 |
| GO:0003429 | Growth plate cartilage chondrocyte morphogenesis | Decreases phenotype | PMID:38060174 |
| GO:0003432 | Cell growth involved in growth plate cartilage chondrocyte morphogenesis | Decreases phenotype | PMID:38060174 |
| GO:0008203 | Cholesterol metabolic process | Affects phenotype | PMID:23517243 |
| GO:0008219 | Cell death | Increases phenotype | PMID:14500569 |
| GO:0009636 | Response to toxic substance | Increases phenotype | PMID:30090431 |
| GO:0015705 | Iodide transport | Decreases phenotype | PMID:30352396 |
| GO:0021884 | Forebrain neuron development | Decreases phenotype | PMID:22987596 |
| GO:0040015 | Negative regulation of multicellular organism growth | Increases phenotype | PMID:30090431 |
| GO:0042403 | Thyroid hormone metabolic process | Affects phenotype | PMID:26517287 |
| GO:0046621 | Negative regulation of organ growth | Increases phenotype | PMID:30090431 |
| GO:0046676 | Negative regulation of insulin secretion | Increases phenotype | PMID:30090431 |
| GO:0070276 | Halogen metabolic process | Affects phenotype | PMID:28054989 |
| GO:0097484 | Dendrite extension | Decreases phenotype | PMID:27444543 |
| GO:1902731 | Negative regulation of chondrocyte proliferation | Decreases phenotype | PMID:38060174 |
| GO:1904214 | Positive regulation of iodide transmembrane transport | Increases phenotype | PMID:22982218 |
| GO:2000609 | Regulation of thyroid hormone generation | Affects phenotype | PMID:29385629 |
| GO:2000610 | Negative regulation of thyroid hormone generation | Increases phenotype | PMID:30090431 |
| GO:2000614 | Positive regulation of thyroid-stimulating hormone secretion | Increases phenotype | PMID:26517287; PMID:38060174 |
| GO:2000854 | Positive regulation of corticosterone secretion | Increases phenotype | PMID:30090431 |
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.