| GO ID | GO name | Interaction type | Reference |
|---|---|---|---|
| GO:0000422 | Autophagy of mitochondrion | Increases phenotype | PMID:24036476 |
| GO:0004197 | Cysteine-type endopeptidase activity | Increases phenotype | PMID:23968587; PMID:31730886; PMID:34302491; PMID:34302491 |
| GO:0004697 | Protein kinase c activity | Increases phenotype | PMID:10484327 |
| GO:0006309 | Apoptotic dna fragmentation | Increases phenotype | PMID:10469363; PMID:10554762; PMID:11093795; PMID:12180275; PMID:12579951; PMID:15909127; PMID:17245372; PMID:21534955; PMID:7949469; PMID:8376790 |
| GO:0006606 | Protein import into nucleus | Affects phenotype | PMID:36534342 |
| GO:0006749 | Glutathione metabolic process | Increases phenotype | PMID:32387680 |
| GO:0006750 | Glutathione biosynthetic process | Affects phenotype | PMID:24912781 |
| GO:0006915 | Apoptotic process | Increases phenotype | PMID:10222263; PMID:10469363; PMID:10486196; PMID:10506188; PMID:10554762; PMID:10663630; PMID:10816077; PMID:11010806; PMID:11093795; PMID:11502879; PMID:15817572; PMID:18451153; PMID:24464939; PMID:30660566; PMID:11853698; PMID:11853698; PMID:19552762; PMID:12180275; PMID:12443983; PMID:12443983; PMID:12871656; PMID:16803879; PMID:20594614; PMID:12579951; PMID:12579951; PMID:16402917; PMID:18451153; PMID:14718647; PMID:14749476; PMID:15217956; PMID:15809080; PMID:15809080; PMID:18451153; PMID:15842767; PMID:15907805; PMID:15909127; PMID:16213648; PMID:16556679; PMID:16927020; PMID:17234824; PMID:18172213; PMID:18182247; PMID:18218830; PMID:18451153; PMID:18451153; PMID:18832097; PMID:18850582; PMID:19406941; PMID:19738048; PMID:19741129; PMID:20003127; PMID:20561156; PMID:21047305; PMID:21933852; PMID:23840623; PMID:24912781; PMID:25586182; PMID:26419736; PMID:26775663; PMID:28223195; PMID:31299294; PMID:32712770; PMID:35158046; PMID:35182693; PMID:8376790; PMID:8844727; PMID:9930745 |
| GO:0006919 | Activation of cysteine-type endopeptidase activity involved in apoptotic process | Increases phenotype | PMID:25841707 |
| GO:0006974 | Cellular response to dna damage stimulus | Increases phenotype | PMID:30660566 |
| GO:0006979 | Response to oxidative stress | Increases phenotype | PMID:20433817 |
| GO:0007049 | Cell cycle | Affects phenotype | PMID:11502879; PMID:9458082; PMID:9858922 |
| GO:0008217 | Regulation of blood pressure | Affects phenotype | PMID:1685570 |
| GO:0008219 | Cell death | Increases phenotype | PMID:11535817; PMID:15665074; PMID:15964487; PMID:17245372; PMID:17245372; PMID:29938581; PMID:20433817; PMID:25704409; PMID:28747609; PMID:29938581 |
| GO:0008234 | Cysteine-type peptidase activity | Increases phenotype | PMID:38748041 |
| GO:0008283 | Cell population proliferation | Affects phenotype | PMID:12169386; PMID:18448488; PMID:20579391; PMID:21223980; PMID:23293585; PMID:26963176; PMID:39674444; PMID:8889840 |
| GO:0008284 | Positive regulation of cell population proliferation | Decreases phenotype | PMID:27539959 |
| GO:0008285 | Negative regulation of cell population proliferation | Increases phenotype | PMID:29933105; PMID:31356851; PMID:35337807; PMID:35483669 |
| GO:0010917 | Negative regulation of mitochondrial membrane potential | Increases phenotype | PMID:31433962 |
| GO:0010918 | Positive regulation of mitochondrial membrane potential | Decreases phenotype | PMID:19002561; PMID:25451566 |
| GO:0010942 | Positive regulation of cell death | Increases phenotype | PMID:25330770; PMID:25426952; PMID:31401084 |
| GO:0016043 | Cellular component organization | Affects phenotype | PMID:35483669 |
| GO:0016505 | Peptidase activator activity involved in apoptotic process | Increases phenotype | PMID:30502353 |
| GO:0018108 | Peptidyl-tyrosine phosphorylation | Increases phenotype | PMID:19814731 |
| GO:0018158 | Protein oxidation | Increases phenotype | PMID:19002561 |
| GO:0030154 | Cell differentiation | Increases phenotype | PMID:1648909 |
| GO:0030182 | Neuron differentiation | Increases phenotype | PMID:23293585; PMID:23329662 |
| GO:0030262 | Apoptotic nuclear changes | Increases phenotype | PMID:34635930 |
| GO:0030263 | Apoptotic chromosome condensation | Increases phenotype | PMID:26124276; PMID:29410032 |
| GO:0030264 | Nuclear fragmentation involved in apoptotic nuclear change | Increases phenotype | PMID:26124276 |
| GO:0032793 | Positive regulation of creb transcription factor activity | Increases phenotype | PMID:17680988 |
| GO:0042310 | Vasoconstriction | Increases phenotype | PMID:8694307; PMID:8764313 |
| GO:0042554 | Superoxide anion generation | Increases phenotype | PMID:9437538 |
| GO:0043065 | Positive regulation of apoptotic process | Increases phenotype | PMID:20133810; PMID:22025197; PMID:22484375; PMID:22484375; PMID:23675469; PMID:29330302; PMID:22484375; PMID:33554279; PMID:26124276; PMID:26124276; PMID:27392949; PMID:30502331; PMID:27539959; PMID:27554043; PMID:29330302; PMID:29341879; PMID:33554279 |
| GO:0044237 | Cellular metabolic process | Affects phenotype | PMID:22108603; PMID:34785303; PMID:34856211; PMID:35158046; PMID:35182693; PMID:37591408; PMID:38191190 |
| GO:0045444 | Fat cell differentiation | Decreases phenotype | PMID:24740755 |
| GO:0045794 | Negative regulation of cell volume | Increases phenotype | PMID:17097791 |
| GO:0046034 | Atp metabolic process | Affects phenotype | PMID:24912781 |
| GO:0050766 | Positive regulation of phagocytosis | Decreases phenotype | PMID:17958546 |
| GO:0051881 | Regulation of mitochondrial membrane potential | Affects phenotype | PMID:21933852; PMID:23293585 |
| GO:0070527 | Platelet aggregation | Increases phenotype | PMID:19814731 |
| GO:0070528 | Protein kinase c signaling | Decreases phenotype | PMID:18313772 |
| GO:0070782 | Phosphatidylserine exposure on apoptotic cell surface | Increases phenotype | PMID:17097791; PMID:19002561 |
| GO:0072593 | Reactive oxygen species metabolic process | Increases phenotype | PMID:23293585 |
| GO:0090023 | Positive regulation of neutrophil chemotaxis | Increases phenotype | PMID:11801740 |
| GO:0090200 | Positive regulation of release of cytochrome c from mitochondria | Increases phenotype | PMID:19002561 |
| GO:0097202 | Activation of cysteine-type endopeptidase activity | Increases phenotype | PMID:25841707 |
| GO:0106041 | Positive regulation of gaba-a receptor activity | Affects phenotype | PMID:29588939 |
| GO:1900020 | Positive regulation of protein kinase c activity | Increases phenotype | PMID:18313772 |
| GO:1901030 | Positive regulation of mitochondrial outer membrane permeabilization involved in apoptotic signaling pathway | Increases phenotype | PMID:19002561 |
| GO:1901988 | Negative regulation of cell cycle phase transition | Increases phenotype | PMID:38275666 |
| GO:1902512 | Positive regulation of apoptotic dna fragmentation | Increases phenotype | PMID:19002561; PMID:26459185; PMID:9751194 |
| GO:1903409 | Reactive oxygen species biosynthetic process | Increases phenotype | PMID:11896666 |
| GO:1903428 | Positive regulation of reactive oxygen species biosynthetic process | Increases phenotype | PMID:19002561 |
| GO:1903955 | Positive regulation of protein targeting to mitochondrion | Increases phenotype | PMID:29410032 |
| GO:1990806 | Ligand-gated ion channel signaling pathway | Decreases phenotype | PMID:29588939 |
| GO:2001171 | Positive regulation of atp biosynthetic process | Decreases phenotype | PMID:28898253 |
| GO:2001272 | Positive regulation of cysteine-type endopeptidase activity involved in execution phase of apoptosis | Increases phenotype | PMID:22639866; PMID:26124276 |
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.