| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0006882 | Cellular zinc ion homeostasis | Affects phenotype | PMID:26026913 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:19591892 |
| GO:0006979 | Response to oxidative stress | Affects phenotype | PMID:24211530 |
| GO:0007224 | Smoothened signaling pathway | Decreases phenotype | PMID:31652400 |
| GO:0016477 | Cell migration | Affects phenotype | PMID:22683935 |
| GO:0036091 | Positive regulation of transcription from rna polymerase ii promoter in response to oxidative stress | Increases phenotype | PMID:32335162 |
| GO:0043525 | Positive regulation of neuron apoptotic process | Increases phenotype | PMID:12782107 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:32870474 |
| GO:0048384 | Retinoic acid receptor signaling pathway | Decreases phenotype | PMID:31652400 |
| GO:0051092 | Positive regulation of nf-kappab transcription factor activity | Increases phenotype | PMID:25752435 |
| GO:0060070 | Canonical wnt signaling pathway | Decreases phenotype | PMID:31652400 |
| GO:1902656 | Calcium ion import into cytosol | Increases phenotype | PMID:12782107 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:25752435 |
| GO:1990138 | Neuron projection extension | 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.