| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0006750 | Glutathione biosynthetic process | Decreases phenotype | PMID:17265426; PMID:27452781 |
| GO:0006919 | Activation of cysteine-type endopeptidase activity involved in apoptotic process | Increases phenotype | PMID:30247689 |
| GO:0016042 | Lipid catabolic process | Decreases phenotype | PMID:27452781 |
| GO:0036211 | Protein modification process | Increases phenotype | PMID:27452781 |
| GO:0045777 | Positive regulation of blood pressure | Increases phenotype | PMID:27452781 |
| GO:0060079 | Excitatory postsynaptic potential | Affects phenotype | PMID:32715571 |
| GO:0061744 | Motor behavior | Decreases phenotype | PMID:30247689 |
| GO:1903980 | Positive regulation of microglial cell activation | Increases phenotype | PMID:30247689 |
| GO:2000673 | Positive regulation of motor neuron apoptotic process | Increases phenotype | PMID:30247689 |
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.