Perfluorodecanoic acid


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000212 Meiotic spindle organization Decreases phenotype PMID:34358620
GO:0003006 Developmental process involved in reproduction Decreases phenotype PMID:34171588
GO:0004021 L-alanine:2-oxoglutarate aminotransferase activity Decreases phenotype PMID:29156323
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:39933620
GO:0005243 Gap junction channel activity Decreases phenotype PMID:26023933
GO:0006119 Oxidative phosphorylation Decreases phenotype PMID:39933620
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:31841032
GO:0006590 Thyroid hormone generation Decreases phenotype PMID:27219111
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:36423729
GO:0006650 Glycerophospholipid metabolic process Affects phenotype PMID:33113464
GO:0006694 Steroid biosynthetic process Affects phenotype PMID:33991873
GO:0006789 Bilirubin conjugation Increases phenotype PMID:38181850
GO:0006915 Apoptotic process Increases phenotype PMID:34358620
GO:0006954 Inflammatory response Decreases phenotype PMID:32916415
GO:0006955 Immune response Decreases phenotype PMID:32772733
GO:0007005 Mitochondrion organization Affects phenotype PMID:34358620
GO:0007015 Actin filament organization Decreases phenotype PMID:34358620
GO:0007128 Meiotic prophase i Decreases phenotype PMID:34358620
GO:0007605 Sensory perception of sound Affects phenotype PMID:32474307
GO:0008219 Cell death Affects phenotype PMID:26599974; PMID:39933616
GO:0008283 Cell population proliferation Affects phenotype PMID:23539207; PMID:8001245
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:35337807
GO:0008652 Amino acid biosynthetic process Affects phenotype PMID:32634666
GO:0010424 Dna methylation on cytosine within a cg sequence Affects phenotype PMID:33356526
GO:0010942 Positive regulation of cell death Increases phenotype PMID:27511595
GO:0015721 Bile acid and bile salt transport Decreases phenotype PMID:38181850
GO:0016049 Cell growth Decreases phenotype PMID:30144469
GO:0016321 Female meiosis chromosome segregation Decreases phenotype PMID:34358620
GO:0019369 Arachidonic acid metabolic process Affects phenotype PMID:33991873
GO:0030072 Peptide hormone secretion Decreases phenotype PMID:31216000
GO:0030282 Bone mineralization Decreases phenotype PMID:35750749
GO:0030308 Negative regulation of cell growth Increases phenotype PMID:36341878
GO:0030431 Sleep Decreases phenotype PMID:39512894
GO:0032204 Regulation of telomere maintenance Affects phenotype PMID:34454526
GO:0032691 Negative regulation of interleukin-1 beta production Increases phenotype PMID:35065522
GO:0034440 Lipid oxidation Affects phenotype PMID:39933620
GO:0035038 Female pronucleus assembly Increases phenotype PMID:34358620
GO:0035937 Estrogen secretion Affects phenotype PMID:39933620
GO:0036109 Alpha-linolenic acid metabolic process Affects phenotype PMID:33991873
GO:0036124 Histone h3-k9 trimethylation Increases phenotype PMID:34358620
GO:0042403 Thyroid hormone metabolic process Affects phenotype PMID:24577800; PMID:33243245
GO:0042593 Glucose homeostasis Affects phenotype PMID:32807188; PMID:33984575
GO:0042701 Progesterone secretion Affects phenotype PMID:39933620
GO:0043045 Dna methylation involved in embryo development Affects phenotype PMID:32653021
GO:0043651 Linoleic acid metabolic process Affects phenotype PMID:33991873
GO:0043974 Histone h3-k27 acetylation Increases phenotype PMID:34358620
GO:0044237 Cellular metabolic process Decreases phenotype PMID:38117326; PMID:38549690
GO:0045444 Fat cell differentiation Increases phenotype PMID:34800597
GO:0045540 Regulation of cholesterol biosynthetic process Affects phenotype PMID:29156323
GO:0046034 Atp metabolic process Affects phenotype PMID:39933620
GO:0048589 Developmental growth Decreases phenotype PMID:26895313
GO:0050000 Chromosome localization Affects phenotype PMID:34358620
GO:0051693 Actin filament capping Decreases phenotype PMID:34358620
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:34358620; PMID:39933620
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:39933620
GO:0060443 Mammary gland morphogenesis Decreases phenotype PMID:27511595
GO:0060669 Embryonic placenta morphogenesis Affects phenotype PMID:33677611
GO:0070162 Adiponectin secretion Decreases phenotype PMID:31216000
GO:0070858 Negative regulation of bile acid biosynthetic process Increases phenotype PMID:38181850
GO:0071736 Igg immunoglobulin complex, circulating Decreases phenotype PMID:27501995
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:34358620; PMID:39933620
GO:0080182 Histone h3-k4 trimethylation Decreases phenotype PMID:34358620
GO:0120189 Positive regulation of bile acid secretion Increases phenotype PMID:38181850
GO:0140042 Lipid droplet formation Increases phenotype PMID:36423729
GO:1903180 Negative regulation of dopamine biosynthetic process Increases phenotype PMID:34371090
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:36075290
GO:1904145 Negative regulation of meiotic cell cycle process involved in oocyte maturation Increases phenotype PMID:34358620
GO:1904358 Positive regulation of telomere maintenance via telomere lengthening Increases phenotype PMID:34193151
GO:2000610 Negative regulation of thyroid hormone generation Increases phenotype PMID:31518930
GO:2000611 Positive regulation of thyroid hormone generation Increases phenotype PMID:31518930
GO:2000613 Negative regulation of thyroid-stimulating hormone secretion Increases phenotype PMID:31518930
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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.