| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0002638 | Negative regulation of immunoglobulin production | Increases phenotype | PMID:24188624 |
| GO:0002639 | Positive regulation of immunoglobulin production | Increases phenotype | PMID:24935097 |
| GO:0002693 | Positive regulation of cellular extravasation | Increases phenotype | PMID:30017638 |
| GO:0002866 | Positive regulation of acute inflammatory response to antigenic stimulus | Increases phenotype | PMID:30017638 |
| GO:0006702 | Androgen biosynthetic process | Decreases phenotype | PMID:27663972 |
| GO:0006805 | Xenobiotic metabolic process | Increases phenotype | PMID:29162470 |
| GO:0007614 | Short-term memory | Increases phenotype | PMID:24982620 |
| GO:0008219 | Cell death | Increases phenotype | PMID:26961610 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:24806340; PMID:24832206; PMID:24835555; PMID:27663972; PMID:28855101 |
| GO:0008284 | Positive regulation of cell population proliferation | Increases phenotype | PMID:28426875; PMID:35307500 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:29149346; PMID:31549662 |
| GO:0008584 | Male gonad development | Affects phenotype | PMID:25048109 |
| GO:0016049 | Cell growth | Decreases phenotype | PMID:36277366 |
| GO:0031324 | Negative regulation of cellular metabolic process | Increases phenotype | PMID:35413382 |
| GO:0031589 | Cell-substrate adhesion | Decreases phenotype | PMID:32466334 |
| GO:0031959 | Mineralocorticoid receptor signaling pathway | Increases phenotype | PMID:29149346 |
| GO:0033148 | Positive regulation of intracellular estrogen receptor signaling pathway | Increases phenotype | PMID:26139245; PMID:27473340 |
| GO:0035847 | Uterine epithelium development | Increases phenotype | PMID:27473340 |
| GO:0035938 | Estradiol secretion | Increases phenotype | PMID:30817981 |
| GO:0040029 | Epigenetic regulation of gene expression | Affects phenotype | PMID:25057798 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:36277366 |
| GO:0045931 | Positive regulation of mitotic cell cycle | Increases phenotype | PMID:35307500 |
| GO:0046622 | Positive regulation of organ growth | Increases phenotype | PMID:27473340 |
| GO:0050769 | Positive regulation of neurogenesis | Increases phenotype | PMID:24982620 |
| GO:0060326 | Cell chemotaxis | Increases phenotype | PMID:32466334 |
| GO:0061370 | Testosterone biosynthetic process | Decreases phenotype | PMID:27663972 |
| GO:0070374 | Positive regulation of erk1 and erk2 cascade | Increases phenotype | PMID:27413106 |
| GO:1900017 | Positive regulation of cytokine production involved in inflammatory response | Increases phenotype | PMID:24935097 |
| GO:1900745 | Positive regulation of p38mapk cascade | Increases phenotype | PMID:27413106 |
| GO:1903047 | Mitotic cell cycle process | Affects phenotype | PMID:32466334 |
| GO:1903365 | Regulation of fear response | Affects phenotype | PMID:24982620 |
| GO:1903709 | Uterine gland development | Increases phenotype | PMID:27473340 |
| GO:1903753 | Negative regulation of p38mapk cascade | Increases phenotype | PMID:35413382 |
| GO:1990349 | Gap junction-mediated intercellular transport | Decreases phenotype | PMID:27413106; PMID:35413382 |
| GO:2000529 | Positive regulation of myeloid dendritic cell chemotaxis | Increases phenotype | PMID:30017638 |
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.