| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0001556 | Oocyte maturation | Decreases phenotype | PMID:34718031 |
| GO:0004602 | Glutathione peroxidase activity | Decreases phenotype | PMID:33577942; PMID:35772596 |
| GO:0004784 | Superoxide dismutase activity | Affects phenotype | PMID:26095701; PMID:33577942 |
| GO:0006534 | Cysteine metabolic process | Affects phenotype | PMID:35772596 |
| GO:0006749 | Glutathione metabolic process | Affects phenotype | PMID:26584762; PMID:33577942; PMID:35772596 |
| GO:0006750 | Glutathione biosynthetic process | Increases phenotype | PMID:30266311 |
| GO:0006884 | Cell volume homeostasis | Affects phenotype | PMID:33217525 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:26095701; PMID:33577942 |
| GO:0007009 | Plasma membrane organization | Affects phenotype | PMID:33217525 |
| GO:0007057 | Spindle assembly involved in female meiosis i | Decreases phenotype | PMID:34718031 |
| GO:0008219 | Cell death | Increases phenotype | PMID:27913847; PMID:27913847; PMID:29604266; PMID:29604266; PMID:35772596 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:27913847 |
| GO:0015811 | L-cystine transport | Affects phenotype | PMID:35772596 |
| GO:0016042 | Lipid catabolic process | Increases phenotype | PMID:26095701 |
| GO:0016567 | Protein ubiquitination | Affects phenotype | PMID:35367319 |
| GO:0018158 | Protein oxidation | Increases phenotype | PMID:26095701; PMID:26584762 |
| GO:0030199 | Collagen fibril organization | Increases phenotype | PMID:34896196 |
| GO:0031619 | Homologous chromosome orientation involved in meiotic metaphase i plate congression | Affects phenotype | PMID:34718031 |
| GO:0032776 | Dna methylation on cytosine | Affects phenotype | PMID:38806716 |
| GO:0033566 | Gamma-tubulin complex localization | Affects phenotype | PMID:34718031 |
| GO:0034440 | Lipid oxidation | Increases phenotype | PMID:26584762; PMID:35772596 |
| GO:0034976 | Response to endoplasmic reticulum stress | Increases phenotype | PMID:25577197 |
| GO:0042554 | Superoxide anion generation | Affects phenotype | PMID:34896196 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:33577942; PMID:33577942; PMID:35772596; PMID:35367319; PMID:35772596 |
| GO:0045454 | Cell redox homeostasis | Decreases phenotype | PMID:26584762 |
| GO:0046034 | Atp metabolic process | Increases phenotype | PMID:33577942 |
| GO:0050000 | Chromosome localization | Affects phenotype | PMID:34718031 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:29604266; PMID:33577942; PMID:34718031 |
| GO:0055072 | Iron ion homeostasis | Affects phenotype | PMID:35772596 |
| GO:0070269 | Pyroptosis | Increases phenotype | PMID:33217525 |
| GO:0070842 | Aggresome assembly | Affects phenotype | PMID:35367319 |
| GO:0070994 | Detection of oxidative stress | Increases phenotype | PMID:35772596 |
| GO:0072593 | Reactive oxygen species metabolic process | Affects phenotype | PMID:33577942; PMID:34718031; PMID:34896196; PMID:35772596 |
| GO:0097212 | Lysosomal membrane organization | Affects phenotype | PMID:33217525 |
| GO:1901671 | Positive regulation of superoxide dismutase activity | Increases phenotype | PMID:26584762 |
| GO:1902177 | Positive regulation of oxidative stress-induced intrinsic apoptotic signaling pathway | Increases phenotype | PMID:25577197 |
| GO:1902237 | Positive regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway | Increases phenotype | PMID:25577197 |
| GO:1903409 | Reactive oxygen species biosynthetic process | Increases phenotype | PMID:29604266 |
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.