Naproxen


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001516 Prostaglandin biosynthetic process Increases phenotype PMID:22155309
GO:0003094 Glomerular filtration Decreases phenotype PMID:2203262
GO:0005980 Glycogen catabolic process Increases phenotype PMID:7713362
GO:0006693 Prostaglandin metabolic process Affects phenotype PMID:25034942
GO:0006749 Glutathione metabolic process Affects phenotype PMID:25034942
GO:0006915 Apoptotic process Increases phenotype PMID:12357301
GO:0006979 Response to oxidative stress Increases phenotype PMID:16472794; PMID:9583089
GO:0007049 Cell cycle Affects phenotype PMID:12357301
GO:0007283 Spermatogenesis Decreases phenotype PMID:25034942
GO:0008217 Regulation of blood pressure Affects phenotype PMID:12152004; PMID:8227469; PMID:9566780
GO:0009636 Response to toxic substance Decreases phenotype PMID:21319177
GO:0010942 Positive regulation of cell death Increases phenotype PMID:28754375
GO:0035812 Renal sodium excretion Decreases phenotype PMID:12152004
GO:0042178 Xenobiotic catabolic process Affects phenotype PMID:16472794
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:7718302; PMID:9583089
GO:0060326 Cell chemotaxis Decreases phenotype PMID:314231; PMID:6853143
GO:0097722 Sperm motility Decreases phenotype PMID:25034942
GO:1904996 Positive regulation of leukocyte adhesion to vascular endothelial cell Increases phenotype PMID:14762100
GO:2001171 Positive regulation of atp biosynthetic process Decreases phenotype PMID:28754375
GO:2001303 Lipoxin a4 biosynthetic process Increases phenotype PMID:14762100

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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.