Mifepristone


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000165 Mapk cascade Increases phenotype PMID:20535544
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:24812154
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:21244764; PMID:7777588; PMID:9326359
GO:0006497 Protein lipidation Increases phenotype PMID:33359579
GO:0006606 Protein import into nucleus Affects phenotype PMID:34273429
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:35589016
GO:0006695 Cholesterol biosynthetic process Affects phenotype PMID:27374722
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:24812154
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:23373965
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:31566189
GO:0006915 Apoptotic process Affects phenotype PMID:11040338; PMID:11311531; PMID:11958592; PMID:12127907; PMID:12645856; PMID:16638347; PMID:17070682; PMID:19339209; PMID:21244764; PMID:30628712; PMID:37009741; PMID:8392561; PMID:8660802; PMID:9326359
GO:0006919 Activation of cysteine-type endopeptidase activity involved in apoptotic process Increases phenotype PMID:38636494
GO:0006979 Response to oxidative stress Increases phenotype PMID:19729004
GO:0007049 Cell cycle Decreases phenotype PMID:17545545
GO:0008217 Regulation of blood pressure Affects phenotype PMID:10100081; PMID:2719105; PMID:3692572
GO:0008219 Cell death Increases phenotype PMID:17123556; PMID:29222744; PMID:2936615
GO:0008283 Cell population proliferation Affects phenotype PMID:16326432; PMID:16525653; PMID:17545545; PMID:16638347; PMID:16707792; PMID:17545545; PMID:18579510; PMID:20363256; PMID:20535544; PMID:22850435; PMID:2683973; PMID:2936615
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:26385866; PMID:32619553
GO:0008610 Lipid biosynthetic process Increases phenotype PMID:24812154; PMID:27003841
GO:0010719 Negative regulation of epithelial to mesenchymal transition Increases phenotype PMID:32619553
GO:0010765 Positive regulation of sodium ion transport Increases phenotype PMID:1328298
GO:0010884 Positive regulation of lipid storage Increases phenotype PMID:29782964
GO:0015908 Fatty acid transport Affects phenotype PMID:35589016
GO:0016042 Lipid catabolic process Increases phenotype PMID:22736252; PMID:24812154
GO:0016049 Cell growth Affects phenotype PMID:30217652
GO:0016477 Cell migration Affects phenotype PMID:19853640; PMID:25763180
GO:0030336 Negative regulation of cell migration Increases phenotype PMID:32619553
GO:0031392 Regulation of prostaglandin biosynthetic process Affects phenotype PMID:2615355
GO:0033555 Multicellular organismal response to stress Decreases phenotype PMID:26289146
GO:0035810 Positive regulation of urine volume Increases phenotype PMID:2719105
GO:0042127 Regulation of cell population proliferation Affects phenotype PMID:2615355
GO:0042307 Positive regulation of protein import into nucleus Increases phenotype PMID:32619553
GO:0042310 Vasoconstriction Increases phenotype PMID:21757059
GO:0042311 Vasodilation Increases phenotype PMID:21757059
GO:0043117 Positive regulation of vascular permeability Increases phenotype PMID:29247675
GO:0043124 Negative regulation of i-kappab kinase/nf-kappab signaling Increases phenotype PMID:32619553
GO:0043280 Positive regulation of cysteine-type endopeptidase activity involved in apoptotic process Increases phenotype PMID:38636494
GO:0043970 Histone h3-k9 acetylation Decreases phenotype PMID:29660438; PMID:30359671; PMID:32663519
GO:0044027 Hypermethylation of cpg island Increases phenotype PMID:37972751
GO:0044237 Cellular metabolic process Decreases phenotype PMID:37009741
GO:0045444 Fat cell differentiation Increases phenotype PMID:24418828
GO:0045599 Negative regulation of fat cell differentiation Increases phenotype PMID:29782964
GO:0046676 Negative regulation of insulin secretion Increases phenotype PMID:32791177
GO:0048386 Positive regulation of retinoic acid receptor signaling pathway Increases phenotype PMID:26820057
GO:0048598 Embryonic morphogenesis Decreases phenotype PMID:26385866
GO:0050847 Progesterone receptor signaling pathway Decreases phenotype PMID:26022396
GO:0050891 Multicellular organismal water homeostasis Decreases phenotype PMID:35786681
GO:0051480 Regulation of cytosolic calcium ion concentration Affects phenotype PMID:27264040
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:17070682; PMID:21244764
GO:0055074 Calcium ion homeostasis Affects phenotype PMID:28324061
GO:0060326 Cell chemotaxis Increases phenotype PMID:7766432
GO:0061370 Testosterone biosynthetic process Decreases phenotype PMID:29902490
GO:0071548 Response to dexamethasone Decreases phenotype PMID:32619553
GO:0086003 Cardiac muscle cell contraction Increases phenotype PMID:28324061
GO:0097154 Gabaergic neuron differentiation Increases phenotype PMID:32445661
GO:0140042 Lipid droplet formation Increases phenotype PMID:35589016
GO:1900181 Negative regulation of protein localization to nucleus Increases phenotype PMID:32619553
GO:1900272 Negative regulation of long-term synaptic potentiation Increases phenotype PMID:26289146
GO:1900273 Positive regulation of long-term synaptic potentiation Decreases phenotype PMID:26289146
GO:1902261 Positive regulation of delayed rectifier potassium channel activity Increases phenotype PMID:16985185
GO:1905962 Glutamatergic neuron differentiation Decreases phenotype PMID:32445661
GO:2000225 Negative regulation of testosterone biosynthetic process Increases phenotype PMID:37972751
GO:2000866 Positive regulation of estradiol secretion Increases phenotype PMID:35786681
GO:2000872 Positive regulation of progesterone secretion Increases phenotype PMID:35786681
GO:2001024 Negative regulation of response to drug Increases phenotype PMID:30229846
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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.