| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001836 | Release of cytochrome c from mitochondria | Increases phenotype | PMID:23535401 |
| GO:0002523 | Leukocyte migration involved in inflammatory response | Increases phenotype | PMID:33749501 |
| GO:0004069 | L-aspartate:2-oxoglutarate aminotransferase activity | Increases phenotype | PMID:33749501 |
| GO:0004129 | Cytochrome-c oxidase activity | Decreases phenotype | PMID:33749501 |
| GO:0004784 | Superoxide dismutase activity | Decreases phenotype | PMID:33749501 |
| GO:0006309 | Apoptotic dna fragmentation | Increases phenotype | PMID:23535401 |
| GO:0006749 | Glutathione metabolic process | Affects phenotype | PMID:33749501 |
| GO:0006750 | Glutathione biosynthetic process | Decreases phenotype | PMID:23535401 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:23535401; PMID:31345100; PMID:33749501 |
| GO:0007005 | Mitochondrion organization | Decreases phenotype | PMID:33749501 |
| GO:0008121 | Ubiquinol-cytochrome-c reductase activity | Decreases phenotype | PMID:33749501 |
| GO:0008137 | Nadh dehydrogenase (ubiquinone) activity | Decreases phenotype | PMID:33749501 |
| GO:0008177 | Succinate dehydrogenase (ubiquinone) activity | Decreases phenotype | PMID:33749501 |
| GO:0008284 | Positive regulation of cell population proliferation | Increases phenotype | PMID:32634517 |
| GO:0009055 | Electron transfer activity | Decreases phenotype | PMID:33749501 |
| GO:0010460 | Positive regulation of heart rate | Increases phenotype | PMID:32634517 |
| GO:0019229 | Regulation of vasoconstriction | Affects phenotype | PMID:32320793 |
| GO:0030263 | Apoptotic chromosome condensation | Increases phenotype | PMID:33749501 |
| GO:0032774 | Rna biosynthetic process | Affects phenotype | PMID:33749501 |
| GO:0042221 | Response to chemical | Increases phenotype | PMID:32634517 |
| GO:0042310 | Vasoconstriction | Increases phenotype | PMID:32320793 |
| GO:0042632 | Cholesterol homeostasis | Decreases phenotype | PMID:32634517 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:31166132 |
| GO:0045776 | Negative regulation of blood pressure | Increases phenotype | PMID:32634517 |
| GO:0045907 | Positive regulation of vasoconstriction | Increases phenotype | PMID:32634517 |
| GO:0046034 | Atp metabolic process | Affects phenotype | PMID:33749501 |
| GO:0046466 | Membrane lipid catabolic process | Increases phenotype | PMID:30426860; PMID:31345100 |
| GO:0070328 | Triglyceride homeostasis | Decreases phenotype | PMID:32634517 |
| GO:0070527 | Platelet aggregation | Affects phenotype | PMID:32634517 |
| GO:0072593 | Reactive oxygen species metabolic process | Increases phenotype | PMID:23535401; PMID:33749501 |
| GO:1903409 | Reactive oxygen species biosynthetic process | Increases phenotype | PMID:31345100 |
| GO:1905144 | Response to acetylcholine | Increases phenotype | PMID:32634517 |
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.