| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000737 | Dna catabolic process, endonucleolytic | Increases phenotype | PMID:34503147 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:23436777; PMID:23436777; PMID:28855101; PMID:34503147 |
| GO:0008284 | Positive regulation of cell population proliferation | Increases phenotype | PMID:26344002; PMID:31939705 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:31939705 |
| GO:0030335 | Positive regulation of cell migration | Increases phenotype | PMID:26344002 |
| GO:0031393 | Negative regulation of prostaglandin biosynthetic process | Increases phenotype | PMID:26359731 |
| GO:0034109 | Homotypic cell-cell adhesion | Increases phenotype | PMID:34503147 |
| GO:0036164 | Cell-abiotic substrate adhesion | Decreases phenotype | PMID:34503147 |
| GO:0045333 | Cellular respiration | Increases phenotype | PMID:34503147 |
| GO:0045793 | Positive regulation of cell size | Increases phenotype | PMID:31939705 |
| GO:0046034 | Atp metabolic process | Affects phenotype | PMID:34503147 |
| GO:0048870 | Cell motility | Increases phenotype | PMID:34503147 |
| GO:1903980 | Positive regulation of microglial cell activation | Increases phenotype | PMID:31939705 |
| GO:1905908 | Positive regulation of amyloid fibril formation | Increases phenotype | PMID:31939705 |
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.