Disulfiram


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000086 G2/m transition of mitotic cell cycle Affects phenotype PMID:34182011
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:34182011; PMID:34830855
GO:0001649 Osteoblast differentiation Decreases phenotype PMID:24496638
GO:0003417 Growth plate cartilage development Decreases phenotype PMID:24496638
GO:0004029 Aldehyde dehydrogenase (nad+) activity Increases phenotype PMID:34242567
GO:0006305 Dna alkylation Increases phenotype PMID:24193513
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:10975995
GO:0006490 Oligosaccharide-lipid intermediate biosynthetic process Affects phenotype PMID:3667605
GO:0006606 Protein import into nucleus Increases phenotype PMID:31378764
GO:0006735 Nadh regeneration Decreases phenotype PMID:24126434
GO:0006749 Glutathione metabolic process Affects phenotype PMID:24126434
GO:0006805 Xenobiotic metabolic process Increases phenotype PMID:27421777
GO:0006882 Cellular zinc ion homeostasis Affects phenotype PMID:32661532
GO:0006909 Phagocytosis Affects phenotype PMID:32712770
GO:0006914 Autophagy Increases phenotype PMID:34182011
GO:0006915 Apoptotic process Increases phenotype PMID:11239917; PMID:12467214; PMID:17026967; PMID:21911303; PMID:23033007; PMID:32712770; PMID:34182011
GO:0006950 Response to stress Affects phenotype PMID:3667605
GO:0006954 Inflammatory response Decreases phenotype PMID:33851234
GO:0006979 Response to oxidative stress Increases phenotype PMID:9678494
GO:0007006 Mitochondrial membrane organization Decreases phenotype PMID:31378764
GO:0007009 Plasma membrane organization Decreases phenotype PMID:38172301
GO:0007224 Smoothened signaling pathway Decreases phenotype PMID:31652400
GO:0008217 Regulation of blood pressure Increases phenotype PMID:920841
GO:0008219 Cell death Increases phenotype PMID:11239917; PMID:17245372; PMID:23033007; PMID:24193513; PMID:2598304; PMID:2840217; PMID:32712770; PMID:8448811
GO:0008283 Cell population proliferation Decreases phenotype PMID:21911303; PMID:23033007; PMID:23499788; PMID:24193513; PMID:34182011; PMID:34830855
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:24690739
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:25320179; PMID:32949729
GO:0010918 Positive regulation of mitochondrial membrane potential Decreases phenotype PMID:24126434; PMID:25446858
GO:0010940 Positive regulation of necrotic cell death Increases phenotype PMID:24126434
GO:0010942 Positive regulation of cell death Increases phenotype PMID:24126434; PMID:25446858
GO:0019046 Release from viral latency Increases phenotype PMID:25822022
GO:0031398 Positive regulation of protein ubiquitination Increases phenotype PMID:24690739
GO:0032930 Positive regulation of superoxide anion generation Increases phenotype PMID:24126434
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:24126434; PMID:24496638; PMID:24690739; PMID:25320179
GO:0044237 Cellular metabolic process Decreases phenotype PMID:31378764; PMID:32712770; PMID:34182011; PMID:36175965; PMID:38172301
GO:0045023 G0 to g1 transition Affects phenotype PMID:34182011
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:24193513; PMID:24496638
GO:0046034 Atp metabolic process Affects phenotype PMID:32949729
GO:0046330 Positive regulation of jnk cascade Increases phenotype PMID:24690739
GO:0046466 Membrane lipid catabolic process Affects phenotype PMID:14646230; PMID:2598304; PMID:2840217
GO:0046931 Pore complex assembly Affects phenotype PMID:32367036; PMID:33851234
GO:0048384 Retinoic acid receptor signaling pathway Decreases phenotype PMID:31652400
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:11239917; PMID:12467214
GO:0060070 Canonical wnt signaling pathway Decreases phenotype PMID:31652400
GO:0061951 Establishment of protein localization to plasma membrane Increases phenotype PMID:30591588
GO:0070265 Necrotic cell death Increases phenotype PMID:32712770
GO:0070269 Pyroptosis Affects phenotype PMID:32367036; PMID:33579316; PMID:33851234
GO:0070370 Cellular heat acclimation Affects phenotype PMID:3487525
GO:0070994 Detection of oxidative stress Increases phenotype PMID:24486436
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:29722447; PMID:32712770; PMID:34182011; PMID:35279910
GO:0090398 Cellular senescence Increases phenotype PMID:34830855
GO:0097502 Mannosylation Affects phenotype PMID:3667605
GO:1900745 Positive regulation of p38mapk cascade Increases phenotype PMID:24690739
GO:1903047 Mitotic cell cycle process Affects phenotype PMID:34182011
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:10865939; PMID:23033007; PMID:28300663
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:25320179; PMID:25446858; PMID:39395750
GO:1903578 Regulation of atp metabolic process Increases phenotype PMID:24126434
GO:1904828 Positive regulation of hydrogen sulfide biosynthetic process Increases phenotype PMID:34242567
GO:1990138 Neuron projection extension Decreases phenotype PMID:31652400
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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.