Perfluoroheptanoic acid


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:39933620
GO:0006119 Oxidative phosphorylation Decreases phenotype PMID:39933620
GO:0007283 Spermatogenesis Decreases phenotype PMID:33220336
GO:0008283 Cell population proliferation Increases phenotype PMID:33220336
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:35337807
GO:0034440 Lipid oxidation Affects phenotype PMID:39933620
GO:0035937 Estrogen secretion Affects phenotype PMID:39933620
GO:0042593 Glucose homeostasis Affects phenotype PMID:33984575
GO:0042701 Progesterone secretion Affects phenotype PMID:39933620
GO:0045444 Fat cell differentiation Increases phenotype PMID:34800597
GO:0046034 Atp metabolic process Affects phenotype PMID:39933620
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:39933620
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:39933620
GO:0060669 Embryonic placenta morphogenesis Affects phenotype PMID:33677611
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:33220336
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:39933620
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:36075290
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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.