| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000084 | Mitotic s phase | Increases phenotype | PMID:30905859 |
| GO:0000086 | G2/m transition of mitotic cell cycle | Increases phenotype | PMID:30905859 |
| GO:0004602 | Glutathione peroxidase activity | Increases phenotype | PMID:34687773 |
| GO:0004784 | Superoxide dismutase activity | Increases phenotype | PMID:34687773 |
| GO:0006006 | Glucose metabolic process | Affects phenotype | PMID:27494769 |
| GO:0006750 | Glutathione biosynthetic process | Affects phenotype | PMID:30905859 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:34687773 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:32244372; PMID:34687773 |
| GO:0007015 | Actin filament organization | Affects phenotype | PMID:34687773 |
| GO:0008219 | Cell death | Increases phenotype | PMID:16020200 |
| GO:0008610 | Lipid biosynthetic process | Affects phenotype | PMID:38735451 |
| GO:0010729 | Positive regulation of hydrogen peroxide biosynthetic process | Increases phenotype | PMID:25863213 |
| GO:0010940 | Positive regulation of necrotic cell death | Increases phenotype | PMID:30500929 |
| GO:0010942 | Positive regulation of cell death | Increases phenotype | PMID:20936652 |
| GO:0032125 | Micronucleus organization | Increases phenotype | PMID:30240729 |
| GO:0034440 | Lipid oxidation | Increases phenotype | PMID:25863213 |
| GO:0043977 | Histone h2a-k5 acetylation | Increases phenotype | PMID:24921660 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:32244372; PMID:34687773 |
| GO:0044319 | Wound healing, spreading of cells | Decreases phenotype | PMID:34687773 |
| GO:0044648 | Histone h3-k4 dimethylation | Increases phenotype | PMID:24921660 |
| GO:0045023 | G0 to g1 transition | Decreases phenotype | PMID:30905859 |
| GO:0045930 | Negative regulation of mitotic cell cycle | Affects phenotype | PMID:30905859 |
| GO:0051493 | Regulation of cytoskeleton organization | Affects phenotype | PMID:27494769 |
| GO:0055091 | Phospholipid homeostasis | Affects phenotype | PMID:38735451 |
| GO:0061572 | Actin filament bundle organization | Affects phenotype | PMID:27494769 |
| GO:0070366 | Regulation of hepatocyte differentiation | Affects phenotype | PMID:30500929 |
| GO:0072593 | Reactive oxygen species metabolic process | Affects phenotype | PMID:34687773 |
| GO:0097421 | Liver regeneration | Affects phenotype | PMID:30500929 |
| GO:0140042 | Lipid droplet formation | Increases phenotype | PMID:30500929; PMID:38735451 |
| GO:1901671 | Positive regulation of superoxide dismutase activity | Decreases phenotype | PMID:25863213 |
| GO:1903284 | Positive regulation of glutathione peroxidase activity | Increases phenotype | PMID:25863213 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:27494769 |
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.