| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000278 | Mitotic cell cycle | Increases phenotype | PMID:16959227 |
| GO:0001774 | Microglial cell activation | Increases phenotype | PMID:31323263 |
| GO:0002027 | Regulation of heart rate | Affects phenotype | PMID:29233027 |
| GO:0002158 | Osteoclast proliferation | Affects phenotype | PMID:32513693 |
| GO:0004035 | Alkaline phosphatase activity | Increases phenotype | PMID:35608386 |
| GO:0004340 | Glucokinase activity | Increases phenotype | PMID:24911673 |
| GO:0004346 | Glucose-6-phosphatase activity | Increases phenotype | PMID:24911673 |
| GO:0004457 | Lactate dehydrogenase activity | Increases phenotype | PMID:35608386 |
| GO:0004679 | Amp-activated protein kinase activity | Decreases phenotype | PMID:34428446 |
| GO:0004743 | Pyruvate kinase activity | Increases phenotype | PMID:24911673 |
| GO:0005980 | Glycogen catabolic process | Increases phenotype | PMID:24911673 |
| GO:0006006 | Glucose metabolic process | Affects phenotype | PMID:35608386 |
| GO:0006089 | Lactate metabolic process | Affects phenotype | PMID:35608386 |
| GO:0006749 | Glutathione metabolic process | Increases phenotype | PMID:29233027; PMID:32621855 |
| GO:0006809 | Nitric oxide biosynthetic process | Increases phenotype | PMID:31323263 |
| GO:0006915 | Apoptotic process | Affects phenotype | PMID:18082193; PMID:20543097; PMID:21056623 |
| GO:0006954 | Inflammatory response | Increases phenotype | PMID:29233027 |
| GO:0006979 | Response to oxidative stress | Increases phenotype | PMID:20543097 |
| GO:0007283 | Spermatogenesis | Decreases phenotype | PMID:32621855 |
| GO:0007612 | Learning | Decreases phenotype | PMID:31323263 |
| GO:0007613 | Memory | Decreases phenotype | PMID:31323263 |
| GO:0008184 | Glycogen phosphorylase activity | Decreases phenotype | PMID:24911673 |
| GO:0008283 | Cell population proliferation | Increases phenotype | PMID:16959227; PMID:21056623 |
| GO:0016042 | Lipid catabolic process | Affects phenotype | PMID:29233027 |
| GO:0019627 | Urea metabolic process | Affects phenotype | PMID:35608386 |
| GO:0030263 | Apoptotic chromosome condensation | Increases phenotype | PMID:29233027 |
| GO:0030282 | Bone mineralization | Increases phenotype | PMID:32513693 |
| GO:0032148 | Activation of protein kinase b activity | Decreases phenotype | PMID:34428446 |
| GO:0033687 | Osteoblast proliferation | Increases phenotype | PMID:32513693 |
| GO:0034440 | Lipid oxidation | Increases phenotype | PMID:32621855 |
| GO:0042310 | Vasoconstriction | Increases phenotype | PMID:16368379 |
| GO:0042311 | Vasodilation | Increases phenotype | PMID:15464333; PMID:16368379 |
| GO:0043065 | Positive regulation of apoptotic process | Increases phenotype | PMID:32621855 |
| GO:0045429 | Positive regulation of nitric oxide biosynthetic process | Increases phenotype | PMID:32621855 |
| GO:0046068 | Cgmp metabolic process | Increases phenotype | PMID:34428446 |
| GO:0046209 | Nitric oxide metabolic process | Affects phenotype | PMID:29233027 |
| GO:0046621 | Negative regulation of organ growth | Increases phenotype | PMID:32621855 |
| GO:0048143 | Astrocyte activation | Increases phenotype | PMID:31323263 |
| GO:0050729 | Positive regulation of inflammatory response | Increases phenotype | PMID:32621855 |
| GO:0050808 | Synapse organization | Decreases phenotype | PMID:31323263 |
| GO:0060048 | Cardiac muscle contraction | Decreases phenotype | PMID:20543097 |
| GO:0060348 | Bone development | Increases phenotype | PMID:32513693 |
| GO:0060612 | Adipose tissue development | Increases phenotype | PMID:20471953 |
| GO:0070265 | Necrotic cell death | Increases phenotype | PMID:29233027 |
| GO:0071902 | Positive regulation of protein serine/threonine kinase activity | Decreases phenotype | PMID:34428446 |
| GO:1901318 | Negative regulation of flagellated sperm motility | Increases phenotype | PMID:32621855 |
| GO:2000844 | Negative regulation of testosterone secretion | Increases phenotype | PMID:32621855 |
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.