Emodin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000084 Mitotic s phase Affects phenotype PMID:36893906
GO:0000266 Mitochondrial fission Increases phenotype PMID:34971761
GO:0000737 Dna catabolic process, endonucleolytic Affects phenotype PMID:36893906
GO:0001836 Release of cytochrome c from mitochondria Increases phenotype PMID:27032576
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:26139382; PMID:35753641
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:34971761
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:26139382
GO:0004679 Amp-activated protein kinase activity Increases phenotype PMID:30517764
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:26139382; PMID:37393915
GO:0006749 Glutathione metabolic process Affects phenotype PMID:22271272; PMID:34492313; PMID:34971761
GO:0006805 Xenobiotic metabolic process Increases phenotype PMID:27989148; PMID:34875353
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:34875353
GO:0006915 Apoptotic process Increases phenotype PMID:14729614; PMID:23848338; PMID:27032576; PMID:34875353; PMID:34971761; PMID:35753641
GO:0006954 Inflammatory response Increases phenotype PMID:34492313
GO:0006997 Nucleus organization Decreases phenotype PMID:34492313
GO:0007204 Positive regulation of cytosolic calcium ion concentration Increases phenotype PMID:19549930
GO:0007283 Spermatogenesis Decreases phenotype PMID:21319176
GO:0007626 Locomotory behavior Decreases phenotype PMID:34492313
GO:0008203 Cholesterol metabolic process Affects phenotype PMID:37023836
GO:0008206 Bile acid metabolic process Affects phenotype PMID:28161596; PMID:35753641
GO:0008283 Cell population proliferation Affects phenotype PMID:14729614; PMID:17886230; PMID:23848338; PMID:23848338; PMID:27032576; PMID:27032576
GO:0008284 Positive regulation of cell population proliferation Affects phenotype PMID:19549930; PMID:27989784
GO:0010718 Positive regulation of epithelial to mesenchymal transition Increases phenotype PMID:27989784
GO:0010917 Negative regulation of mitochondrial membrane potential Increases phenotype PMID:37393915
GO:0010918 Positive regulation of mitochondrial membrane potential Decreases phenotype PMID:25448808
GO:0010940 Positive regulation of necrotic cell death Increases phenotype PMID:19549930
GO:0010942 Positive regulation of cell death Increases phenotype PMID:28161596
GO:0015721 Bile acid and bile salt transport Decreases phenotype PMID:28161596
GO:0016049 Cell growth Decreases phenotype PMID:23212659
GO:0030186 Melatonin metabolic process Decreases phenotype PMID:27633141
GO:0030199 Collagen fibril organization Increases phenotype PMID:37023836
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:34492313
GO:0032782 Bile acid secretion Affects phenotype PMID:35753641
GO:0033212 Iron import into cell Increases phenotype PMID:37393915
GO:0042307 Positive regulation of protein import into nucleus Increases phenotype PMID:27989784
GO:0042438 Melanin biosynthetic process Decreases phenotype PMID:26972667
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:21319176; PMID:25448808
GO:0044237 Cellular metabolic process Decreases phenotype PMID:34492313; PMID:34492313; PMID:35753641; PMID:34971761; PMID:36343798; PMID:36893906
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:22271272; PMID:37393915
GO:0045746 Negative regulation of notch signaling pathway Increases phenotype PMID:27989784
GO:0045747 Positive regulation of notch signaling pathway Increases phenotype PMID:27989784
GO:0048266 Behavioral response to pain Increases phenotype PMID:36184831
GO:0050966 Detection of mechanical stimulus involved in sensory perception of pain Increases phenotype PMID:36184831
GO:0050996 Positive regulation of lipid catabolic process Increases phenotype PMID:37393915
GO:0051092 Positive regulation of nf-kappab transcription factor activity Affects phenotype PMID:19549930
GO:0051560 Mitochondrial calcium ion homeostasis Affects phenotype PMID:34971761
GO:0051881 Regulation of mitochondrial membrane potential Decreases phenotype PMID:14729614; PMID:27032576; PMID:34492313; PMID:34875353; PMID:34971761
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:34971761
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:34492313; PMID:34875353; PMID:36184831
GO:0090200 Positive regulation of release of cytochrome c from mitochondria Increases phenotype PMID:25448808
GO:0140042 Lipid droplet formation Increases phenotype PMID:37023836
GO:0160020 Positive regulation of ferroptosis Increases phenotype PMID:37393915
GO:1900017 Positive regulation of cytokine production involved in inflammatory response Increases phenotype PMID:30517764
GO:1900409 Positive regulation of cellular response to oxidative stress Increases phenotype PMID:37393915
GO:1900573 Emodin metabolic process Affects phenotype PMID:36332690
GO:1901318 Negative regulation of flagellated sperm motility Increases phenotype PMID:21319176
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:22271272
GO:1901687 Glutathione derivative biosynthetic process Decreases phenotype PMID:22271272
GO:1902512 Positive regulation of apoptotic dna fragmentation Increases phenotype PMID:19549930
GO:1903047 Mitotic cell cycle process Affects phenotype PMID:36893906
GO:1903283 Negative regulation of glutathione peroxidase activity Increases phenotype PMID:22271272
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:26169035
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:19549930; PMID:37393915
GO:1990961 Xenobiotic detoxification by transmembrane export across the plasma membrane Increases phenotype PMID:19549930
GO:2000391 Positive regulation of neutrophil extravasation Increases phenotype PMID:30517764
DISCLAIMER

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.