Heptachlor


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006749 Glutathione metabolic process Increases phenotype PMID:30719927
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:28531659
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:32949729
GO:0010424 Dna methylation on cytosine within a cg sequence Affects phenotype PMID:34516295
GO:0010718 Positive regulation of epithelial to mesenchymal transition Increases phenotype PMID:30719927
GO:0010976 Positive regulation of neuron projection development Increases phenotype PMID:28385489
GO:0016174 Nad(p)h oxidase h2o2-forming activity Increases phenotype PMID:30719927
GO:0022904 Respiratory electron transport chain Decreases phenotype PMID:25926417
GO:0033148 Positive regulation of intracellular estrogen receptor signaling pathway Increases phenotype PMID:26022396; PMID:26139245
GO:0034440 Lipid oxidation Increases phenotype PMID:30719927
GO:0042554 Superoxide anion generation Affects phenotype PMID:31923579
GO:0043433 Negative regulation of dna-binding transcription factor activity Increases phenotype PMID:26022396
GO:0046034 Atp metabolic process Affects phenotype PMID:32949729
GO:0046323 Glucose import Affects phenotype PMID:31923579
GO:0050847 Progesterone receptor signaling pathway Decreases phenotype PMID:26022396
GO:0070995 Nadph oxidation Increases phenotype PMID:30719927
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:31923579
GO:1900182 Positive regulation of protein localization to nucleus Increases phenotype PMID:30719927
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:30719927
GO:1903788 Positive regulation of glutathione biosynthetic process Increases phenotype PMID:30719927
GO:2001057 Reactive nitrogen species metabolic process Affects phenotype PMID:31923579
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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.