| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000266 | Mitochondrial fission | Affects phenotype | PMID:35158046 |
| GO:0001649 | Osteoblast differentiation | Decreases phenotype | PMID:28017615 |
| GO:0004030 | Aldehyde dehydrogenase [nad(p)+] activity | Decreases phenotype | PMID:35158046 |
| GO:0004035 | Alkaline phosphatase activity | Decreases phenotype | PMID:28017615 |
| GO:0004069 | L-aspartate:2-oxoglutarate aminotransferase activity | Increases phenotype | PMID:35158046 |
| GO:0005739 | Mitochondrion | Increases phenotype | PMID:35158046 |
| GO:0006117 | Acetaldehyde metabolic process | Affects phenotype | PMID:30255327; PMID:34830855; PMID:39988212 |
| GO:0006749 | Glutathione metabolic process | Increases phenotype | PMID:35595033 |
| GO:0006750 | Glutathione biosynthetic process | Decreases phenotype | PMID:28017615 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:35158046 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:35595033 |
| GO:0010942 | Positive regulation of cell death | Increases phenotype | PMID:28821405 |
| GO:0014063 | Negative regulation of serotonin secretion | Increases phenotype | PMID:26711020 |
| GO:0016042 | Lipid catabolic process | Increases phenotype | PMID:28017615; PMID:35158046 |
| GO:0032125 | Micronucleus organization | Increases phenotype | PMID:29110037 |
| GO:0033602 | Negative regulation of dopamine secretion | Increases phenotype | PMID:26711020 |
| GO:0034440 | Lipid oxidation | Increases phenotype | PMID:35595033 |
| GO:0036211 | Protein modification process | Increases phenotype | PMID:28119953 |
| GO:0042310 | Vasoconstriction | Increases phenotype | PMID:2727987 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:35158046 |
| GO:0045930 | Negative regulation of mitotic cell cycle | Increases phenotype | PMID:29110037 |
| GO:0046034 | Atp metabolic process | Affects phenotype | PMID:35158046 |
| GO:0051560 | Mitochondrial calcium ion homeostasis | Affects phenotype | PMID:35158046 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:35158046 |
| GO:0055072 | Iron ion homeostasis | Decreases phenotype | PMID:35595033 |
| GO:0070994 | Detection of oxidative stress | Increases phenotype | PMID:28017615 |
| GO:0072593 | Reactive oxygen species metabolic process | Affects phenotype | PMID:35158046 |
| GO:0150032 | Positive regulation of protein localization to lysosome | Increases phenotype | PMID:35595033 |
| GO:0160020 | Positive regulation of ferroptosis | Increases phenotype | PMID:35595033 |
| GO:1901525 | Negative regulation of mitophagy | Increases phenotype | PMID:35595033 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:35595033 |
| GO:2000786 | Positive regulation of autophagosome assembly | Increases phenotype | PMID:35595033 |
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.