| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0002523 | Leukocyte migration involved in inflammatory response | Increases phenotype | PMID:28689766; PMID:39848458; PMID:39848458 |
| GO:0003105 | Negative regulation of glomerular filtration | Increases phenotype | PMID:28689766 |
| GO:0003300 | Cardiac muscle hypertrophy | Increases phenotype | PMID:33645892 |
| GO:0004021 | L-alanine:2-oxoglutarate aminotransferase activity | Increases phenotype | PMID:39848458 |
| GO:0004035 | Alkaline phosphatase activity | Increases phenotype | PMID:39848458 |
| GO:0004069 | L-aspartate:2-oxoglutarate aminotransferase activity | Increases phenotype | PMID:28499616; PMID:39848458; PMID:39848458 |
| GO:0004111 | Creatine kinase activity | Increases phenotype | PMID:28499616 |
| GO:0004457 | Lactate dehydrogenase activity | Increases phenotype | PMID:28499616 |
| GO:0004602 | Glutathione peroxidase activity | Decreases phenotype | PMID:39848458 |
| GO:0004784 | Superoxide dismutase activity | Decreases phenotype | PMID:39848458 |
| GO:0006304 | Dna modification | Increases phenotype | PMID:39848458 |
| GO:0006629 | Lipid metabolic process | Affects phenotype | PMID:33645892 |
| GO:0006641 | Triglyceride metabolic process | Affects phenotype | PMID:33645892 |
| GO:0006695 | Cholesterol biosynthetic process | Increases phenotype | PMID:28689766 |
| GO:0006754 | Atp biosynthetic process | Decreases phenotype | PMID:27317026 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:25550769 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:33645892 |
| GO:0006979 | Response to oxidative stress | Increases phenotype | PMID:31618080 |
| GO:0007033 | Vacuole organization | Increases phenotype | PMID:28499616 |
| GO:0008203 | Cholesterol metabolic process | Affects phenotype | PMID:33645892 |
| GO:0008219 | Cell death | Increases phenotype | PMID:27317026; PMID:28499616; PMID:28689766 |
| GO:0016042 | Lipid catabolic process | Decreases phenotype | PMID:28499616; PMID:28689766; PMID:33645892 |
| GO:0016049 | Cell growth | Increases phenotype | PMID:28499616 |
| GO:0018158 | Protein oxidation | Affects phenotype | PMID:28499616; PMID:33645892 |
| GO:0019627 | Urea metabolic process | Affects phenotype | PMID:39848458 |
| GO:0030199 | Collagen fibril organization | Increases phenotype | PMID:33645892 |
| GO:0030263 | Apoptotic chromosome condensation | Increases phenotype | PMID:39848458 |
| GO:0030431 | Sleep | Increases phenotype | PMID:27641627 |
| GO:0032769 | Negative regulation of monooxygenase activity | Increases phenotype | PMID:29100959 |
| GO:0042415 | Norepinephrine metabolic process | Affects phenotype | PMID:27641627 |
| GO:0042428 | Serotonin metabolic process | Affects phenotype | PMID:27641627 |
| GO:0046323 | Glucose import | Increases phenotype | PMID:27317026 |
| GO:0046415 | Urate metabolic process | Affects phenotype | PMID:28689766 |
| GO:0046449 | Creatinine metabolic process | Affects phenotype | PMID:39848458 |
| GO:0046466 | Membrane lipid catabolic process | Increases phenotype | PMID:31618080 |
| GO:0051350 | Negative regulation of lyase activity | Increases phenotype | PMID:29100959 |
| GO:0070265 | Necrotic cell death | Increases phenotype | PMID:39848458 |
| GO:0070994 | Detection of oxidative stress | Increases phenotype | PMID:39848458 |
| GO:0090032 | Negative regulation of steroid hormone biosynthetic process | Increases phenotype | PMID:29100959 |
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.