Chloranil


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000080 Mitotic g1 phase Decreases phenotype PMID:30905860
GO:0000084 Mitotic s phase Increases phenotype PMID:30905860
GO:0000730 Dna recombinase assembly Increases phenotype PMID:27989139
GO:0001774 Microglial cell activation Increases phenotype PMID:28238930
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:25123790
GO:0006750 Glutathione biosynthetic process Increases phenotype PMID:30905860
GO:0006751 Glutathione catabolic process Increases phenotype PMID:25742418
GO:0006915 Apoptotic process Increases phenotype PMID:30905860
GO:0008219 Cell death Increases phenotype PMID:28238930
GO:0008283 Cell population proliferation Decreases phenotype PMID:30905860
GO:0010918 Positive regulation of mitochondrial membrane potential Decreases phenotype PMID:28823167
GO:0010942 Positive regulation of cell death Increases phenotype PMID:27989139
GO:0016049 Cell growth Decreases phenotype PMID:30378427
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:28238930
GO:0032461 Positive regulation of protein oligomerization Increases phenotype PMID:28823167
GO:0032596 Protein transport into membrane raft Increases phenotype PMID:27413111
GO:0034976 Response to endoplasmic reticulum stress Increases phenotype PMID:27484784
GO:0036091 Positive regulation of transcription from rna polymerase ii promoter in response to oxidative stress Increases phenotype PMID:25742418
GO:0042116 Macrophage activation Increases phenotype PMID:27413111
GO:0042307 Positive regulation of protein import into nucleus Affects phenotype PMID:27989139
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:27484784; PMID:27484784; PMID:28823167; PMID:27989139
GO:0045930 Negative regulation of mitotic cell cycle Affects phenotype PMID:30905860
GO:0046827 Positive regulation of protein export from nucleus Increases phenotype PMID:27393035
GO:0048143 Astrocyte activation Increases phenotype PMID:27413111
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:30905860
GO:0070585 Protein localization to mitochondrion Increases phenotype PMID:28823167
GO:0070997 Neuron death Increases phenotype PMID:27413111
GO:0071550 Death-inducing signaling complex assembly Increases phenotype PMID:27484784
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:24214992
GO:0090200 Positive regulation of release of cytochrome c from mitochondria Increases phenotype PMID:28823167
GO:0097345 Mitochondrial outer membrane permeabilization Increases phenotype PMID:28823167
GO:1900227 Positive regulation of nlrp3 inflammasome complex assembly Increases phenotype PMID:26901245
GO:1901216 Positive regulation of neuron death Increases phenotype PMID:28823167
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:30905860
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:27484784
GO:1903513 Endoplasmic reticulum to cytosol transport Increases phenotype PMID:28823167
GO:1905898 Positive regulation of response to endoplasmic reticulum stress Increases phenotype PMID:28823167
GO:2000871 Negative regulation of progesterone secretion Increases phenotype PMID:38555059
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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.