| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0002156 | Negative regulation of thyroid hormone mediated signaling pathway | Increases phenotype | PMID:31476497 |
| GO:0002157 | Positive regulation of thyroid hormone mediated signaling pathway | Increases phenotype | PMID:31476497 |
| GO:0003712 | Transcription coregulator activity | Increases phenotype | PMID:35483669 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:19591892 |
| GO:0007224 | Smoothened signaling pathway | Decreases phenotype | PMID:31652400 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:28709983 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:35483669 |
| GO:0016043 | Cellular component organization | Affects phenotype | PMID:35483669 |
| GO:0016505 | Peptidase activator activity involved in apoptotic process | Increases phenotype | PMID:28709983 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:33929904 |
| GO:0045444 | Fat cell differentiation | Increases phenotype | PMID:32473317 |
| GO:0048384 | Retinoic acid receptor signaling pathway | Decreases phenotype | PMID:31652400 |
| GO:0048386 | Positive regulation of retinoic acid receptor signaling pathway | Increases phenotype | PMID:35483669 |
| GO:0060070 | Canonical wnt signaling pathway | Decreases phenotype | PMID:31652400 |
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.