| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001836 | Release of cytochrome c from mitochondria | Increases phenotype | PMID:29935161 |
| GO:0004457 | Lactate dehydrogenase activity | Increases phenotype | PMID:28559121; PMID:28559121; PMID:29621559; PMID:29621559; PMID:31029751 |
| GO:0006590 | Thyroid hormone generation | Decreases phenotype | PMID:21106438; PMID:27114094 |
| GO:0006754 | Atp biosynthetic process | Decreases phenotype | PMID:29935161 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:28559121; PMID:28559121; PMID:29621559; PMID:29621559; PMID:29935161; PMID:31029751 |
| GO:0007029 | Endoplasmic reticulum organization | Decreases phenotype | PMID:31029751 |
| GO:0007612 | Learning | Decreases phenotype | PMID:32521479 |
| GO:0008284 | Positive regulation of cell population proliferation | Increases phenotype | PMID:30796839 |
| GO:0008610 | Lipid biosynthetic process | Decreases phenotype | PMID:27285825 |
| GO:0033148 | Positive regulation of intracellular estrogen receptor signaling pathway | Increases phenotype | PMID:30796839 |
| GO:0048589 | Developmental growth | Decreases phenotype | PMID:27285825 |
| GO:0051402 | Neuron apoptotic process | Increases phenotype | PMID:31029751 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:29935161 |
| GO:1903409 | Reactive oxygen species biosynthetic process | Increases phenotype | PMID:29935161 |
| GO:1904358 | Positive regulation of telomere maintenance via telomere lengthening | Increases phenotype | PMID:34193151 |
| GO:2000609 | Regulation of thyroid hormone generation | Affects phenotype | PMID:39626304 |
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.