| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000080 | Mitotic g1 phase | Affects phenotype | PMID:32278510 |
| GO:0000086 | G2/m transition of mitotic cell cycle | Decreases phenotype | PMID:16427046 |
| GO:0001503 | Ossification | Decreases phenotype | PMID:39531065 |
| GO:0002320 | Lymphoid progenitor cell differentiation | Decreases phenotype | PMID:39331569 |
| GO:0006306 | Dna methylation | Affects phenotype | PMID:17686055; PMID:17686055; PMID:18790780; PMID:18033690; PMID:18790780; PMID:18790780; PMID:20861661; PMID:3258330; PMID:6159882; PMID:6197180; PMID:7511991 |
| GO:0006309 | Apoptotic dna fragmentation | Increases phenotype | PMID:1282508; PMID:7686540; PMID:7686540 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:1282508; PMID:7686540; PMID:18443271; PMID:18829727; PMID:25953102; PMID:32278510 |
| GO:0006954 | Inflammatory response | Increases phenotype | PMID:28392331 |
| GO:0007049 | Cell cycle | Decreases phenotype | PMID:20607034; PMID:7679929 |
| GO:0008219 | Cell death | Increases phenotype | PMID:24518598; PMID:27099147 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:20607034; PMID:25953102; PMID:39531065; PMID:7679929 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:29200404 |
| GO:0010424 | Dna methylation on cytosine within a cg sequence | Decreases phenotype | PMID:33536392 |
| GO:0010918 | Positive regulation of mitochondrial membrane potential | Decreases phenotype | PMID:28942281 |
| GO:0010942 | Positive regulation of cell death | Increases phenotype | PMID:25015661 |
| GO:0019627 | Urea metabolic process | Increases phenotype | PMID:27590069 |
| GO:0030154 | Cell differentiation | Decreases phenotype | PMID:18033690 |
| GO:0031175 | Neuron projection development | Decreases phenotype | PMID:33454822 |
| GO:0032776 | Dna methylation on cytosine | Increases phenotype | PMID:33454822 |
| GO:0042554 | Superoxide anion generation | Increases phenotype | PMID:32278510 |
| GO:0042692 | Muscle cell differentiation | Increases phenotype | PMID:28298639 |
| GO:0043065 | Positive regulation of apoptotic process | Increases phenotype | PMID:9813173 |
| GO:0043525 | Positive regulation of neuron apoptotic process | Increases phenotype | PMID:16427046 |
| GO:0043970 | Histone h3-k9 acetylation | Decreases phenotype | PMID:32278510 |
| GO:0044028 | Dna hypomethylation | Increases phenotype | PMID:27132804 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:32278510 |
| GO:0048386 | Positive regulation of retinoic acid receptor signaling pathway | Increases phenotype | PMID:26820057 |
| GO:0060612 | Adipose tissue development | Increases phenotype | PMID:3891103 |
| GO:0070265 | Necrotic cell death | Increases phenotype | PMID:32278510 |
| GO:0070368 | Positive regulation of hepatocyte differentiation | Increases phenotype | PMID:27590069 |
| GO:0072593 | Reactive oxygen species metabolic process | Affects phenotype | PMID:32278510 |
| GO:0072677 | Eosinophil migration | Increases phenotype | PMID:28392331 |
| GO:0072719 | Cellular response to cisplatin | Increases phenotype | PMID:36336710 |
| GO:0090398 | Cellular senescence | Increases phenotype | PMID:39531065 |
| GO:1901537 | Positive regulation of dna demethylation | Affects phenotype | PMID:33536392 |
| GO:1903047 | Mitotic cell cycle process | Affects phenotype | PMID:32278510 |
| GO:1990138 | Neuron projection extension | Decreases phenotype | PMID:31652400 |
| GO:2001170 | Negative regulation of atp biosynthetic process | Increases phenotype | PMID:28942281 |
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.