| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000165 | Mapk cascade | Increases phenotype | PMID:20804743 |
| GO:0001836 | Release of cytochrome c from mitochondria | Increases phenotype | PMID:37431890 |
| GO:0006309 | Apoptotic dna fragmentation | Increases phenotype | PMID:18851957; PMID:20804743 |
| GO:0006915 | Apoptotic process | Affects phenotype | PMID:14996430; PMID:18851957; PMID:20804743; PMID:33775688; PMID:9921918 |
| GO:0006979 | Response to oxidative stress | Decreases phenotype | PMID:16331539; PMID:18787510 |
| GO:0007049 | Cell cycle | Increases phenotype | PMID:7598686; PMID:8463339; PMID:9188632 |
| GO:0008217 | Regulation of blood pressure | Increases phenotype | PMID:14970111 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:11788567; PMID:1709825; PMID:7598686 |
| GO:0008284 | Positive regulation of cell population proliferation | Increases phenotype | PMID:11843059 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:11843059 |
| GO:0010942 | Positive regulation of cell death | Increases phenotype | PMID:26851681 |
| GO:0016042 | Lipid catabolic process | Increases phenotype | PMID:36690085 |
| GO:0016209 | Antioxidant activity | Decreases phenotype | PMID:36690085 |
| GO:0030154 | Cell differentiation | Increases phenotype | PMID:7598686 |
| GO:0030595 | Leukocyte chemotaxis | Increases phenotype | PMID:1976392; PMID:3674202 |
| GO:0034440 | Lipid oxidation | Increases phenotype | PMID:29077241 |
| GO:0042088 | T-helper 1 type immune response | Decreases phenotype | PMID:7589090 |
| GO:0042119 | Neutrophil activation | Increases phenotype | PMID:19697996 |
| GO:0042310 | Vasoconstriction | Decreases phenotype | PMID:1411948 |
| GO:0042311 | Vasodilation | Increases phenotype | PMID:1411948; PMID:7528848 |
| GO:0042391 | Regulation of membrane potential | Decreases phenotype | PMID:8308680 |
| GO:0042593 | Glucose homeostasis | Decreases phenotype | PMID:29077241 |
| GO:0043299 | Leukocyte degranulation | Affects phenotype | PMID:17880773; PMID:1976392 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:33775688 |
| GO:0044319 | Wound healing, spreading of cells | Decreases phenotype | PMID:33775688 |
| GO:0045333 | Cellular respiration | Increases phenotype | PMID:19697996 |
| GO:0046058 | Camp metabolic process | Affects phenotype | PMID:37431890 |
| GO:0046415 | Urate metabolic process | Decreases phenotype | PMID:32777238 |
| GO:0046449 | Creatinine metabolic process | Decreases phenotype | PMID:32777238 |
| GO:0046466 | Membrane lipid catabolic process | Decreases phenotype | PMID:15932791 |
| GO:0046649 | Lymphocyte activation | Decreases phenotype | PMID:17880773 |
| GO:0048266 | Behavioral response to pain | Decreases phenotype | PMID:37431890 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:18851957; PMID:20620236; PMID:37431890 |
| GO:0070301 | Cellular response to hydrogen peroxide | Increases phenotype | PMID:29077241 |
| GO:0072593 | Reactive oxygen species metabolic process | Affects phenotype | PMID:33775688 |
| GO:1903283 | Negative regulation of glutathione peroxidase activity | Increases phenotype | PMID:29077241 |
| GO:2000562 | Negative regulation of cd4-positive, alpha-beta t cell proliferation | Increases phenotype | PMID:25433234 |
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.