| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:27853103 |
| GO:0008283 | Cell population proliferation | Decreases phenotype | PMID:27853103 |
| GO:0008361 | Regulation of cell size | Affects phenotype | PMID:26391574 |
| GO:0010424 | Dna methylation on cytosine within a cg sequence | Affects phenotype | PMID:34523531 |
| GO:0010918 | Positive regulation of mitochondrial membrane potential | Decreases phenotype | PMID:25160872 |
| GO:0010940 | Positive regulation of necrotic cell death | Increases phenotype | PMID:26391574 |
| GO:0018910 | Benzene metabolic process | Affects phenotype | PMID:38734222 |
| GO:0043065 | Positive regulation of apoptotic process | Increases phenotype | PMID:25160872; PMID:26391574 |
| GO:0043396 | Corticotropin-releasing hormone secretion | Decreases phenotype | PMID:30940137 |
| GO:0045333 | Cellular respiration | Decreases phenotype | PMID:32910239 |
| GO:0046466 | Membrane lipid catabolic process | Increases phenotype | PMID:26391574 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:27853103 |
| GO:1902237 | Positive regulation of endoplasmic reticulum stress-induced intrinsic apoptotic signaling pathway | Increases phenotype | PMID:25160872 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:26391574 |
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.