| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0002027 | Regulation of heart rate | Decreases phenotype | PMID:6707926 |
| GO:0003254 | Regulation of membrane depolarization | Affects phenotype | PMID:37838252 |
| GO:0004497 | Monooxygenase activity | Affects phenotype | PMID:26466350 |
| GO:0008217 | Regulation of blood pressure | Decreases phenotype | PMID:6707926; PMID:7252851 |
| GO:0010890 | Positive regulation of sequestering of triglyceride | Increases phenotype | PMID:29551354 |
| GO:0016042 | Lipid catabolic process | Increases phenotype | PMID:30922767 |
| GO:0018158 | Protein oxidation | Increases phenotype | PMID:30922767 |
| GO:0019226 | Transmission of nerve impulse | Affects phenotype | PMID:26498506 |
| GO:0031987 | Locomotion involved in locomotory behavior | Decreases phenotype | PMID:30922767 |
| GO:0032148 | Activation of protein kinase b activity | Increases phenotype | PMID:29551354 |
| GO:0042416 | Dopamine biosynthetic process | Decreases phenotype | PMID:26466350; PMID:30922767 |
| GO:0042420 | Dopamine catabolic process | Increases phenotype | PMID:30922767 |
| GO:0042421 | Norepinephrine biosynthetic process | Affects phenotype | PMID:26466350 |
| GO:0042593 | Glucose homeostasis | Decreases phenotype | PMID:29551354 |
| GO:0045793 | Positive regulation of cell size | Increases phenotype | PMID:29551354 |
| GO:0055089 | Fatty acid homeostasis | Decreases phenotype | PMID:29551354 |
| GO:0060079 | Excitatory postsynaptic potential | Decreases phenotype | PMID:18216231 |
| GO:0060080 | Inhibitory postsynaptic potential | Decreases phenotype | PMID:11790512 |
| GO:0070328 | Triglyceride homeostasis | Decreases phenotype | PMID:29551354 |
| GO:0070345 | Negative regulation of fat cell proliferation | Increases phenotype | PMID:29551354 |
| GO:0097280 | Histamine secretion mediated by immunoglobulin | Decreases phenotype | PMID:7683115 |
| GO:1903409 | Reactive oxygen species biosynthetic process | Increases phenotype | PMID:30922767 |
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.