| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0003016 | Respiratory system process | Affects phenotype | PMID:24726979 |
| GO:0003993 | Acid phosphatase activity | Decreases phenotype | PMID:33226166 |
| GO:0006007 | Glucose catabolic process | Increases phenotype | PMID:24726979 |
| GO:0006096 | Glycolytic process | Increases phenotype | PMID:32607615 |
| GO:0006633 | Fatty acid biosynthetic process | Decreases phenotype | PMID:24726979 |
| GO:0006641 | Triglyceride metabolic process | Affects phenotype | PMID:32810590 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:19591892 |
| GO:0007204 | Positive regulation of cytosolic calcium ion concentration | Increases phenotype | PMID:30629953 |
| GO:0008121 | Ubiquinol-cytochrome-c reductase activity | Decreases phenotype | PMID:24726979 |
| GO:0008219 | Cell death | Increases phenotype | PMID:29294346 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:33226166; PMID:34642769 |
| GO:0019432 | Triglyceride biosynthetic process | Affects phenotype | PMID:24726979 |
| GO:0030185 | Nitric oxide transport | Affects phenotype | PMID:33226166 |
| GO:0044237 | Cellular metabolic process | Decreases phenotype | PMID:32607615 |
| GO:0045333 | Cellular respiration | Decreases phenotype | PMID:24726979; PMID:32607615; PMID:33512557 |
| GO:0046034 | Atp metabolic process | Affects phenotype | PMID:34642769 |
| GO:0046323 | Glucose import | Increases phenotype | PMID:24726979 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:32607615; PMID:32607615; PMID:34642769; PMID:33512557 |
| GO:1900534 | Palmitic acid catabolic process | Increases phenotype | PMID:24726979 |
| GO:1902632 | Positive regulation of membrane hyperpolarization | Increases phenotype | PMID:30629953 |
| GO:1904181 | Positive regulation of membrane depolarization | Increases phenotype | PMID:30629953 |
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.