beta-Naphthoflavone


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004364 Glutathione transferase activity Increases phenotype PMID:9794803
GO:0006260 Dna replication Increases phenotype PMID:32435917
GO:0006304 Dna modification Increases phenotype PMID:10647909
GO:0006606 Protein import into nucleus Affects phenotype PMID:39480548; PMID:39832710
GO:0006725 Cellular aromatic compound metabolic process Increases phenotype PMID:24140465
GO:0006805 Xenobiotic metabolic process Increases phenotype PMID:19903449; PMID:27159630; PMID:9429083
GO:0006882 Cellular zinc ion homeostasis Affects phenotype PMID:31588062
GO:0006915 Apoptotic process Increases phenotype PMID:27286660
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:30842367
GO:0006979 Response to oxidative stress Increases phenotype PMID:15621696
GO:0008209 Androgen metabolic process Increases phenotype PMID:19903449
GO:0008283 Cell population proliferation Affects phenotype PMID:25370011
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:26593447
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:30373287
GO:0010759 Positive regulation of macrophage chemotaxis Increases phenotype PMID:29180065
GO:0010942 Positive regulation of cell death Increases phenotype PMID:8014883
GO:0016525 Negative regulation of angiogenesis Increases phenotype PMID:29180065
GO:0018411 Protein glucuronidation Increases phenotype PMID:36549901
GO:0030335 Positive regulation of cell migration Decreases phenotype PMID:26593447
GO:0031323 Regulation of cellular metabolic process Affects phenotype PMID:28965233
GO:0032125 Micronucleus organization Increases phenotype PMID:30842367
GO:0032736 Positive regulation of interleukin-13 production Affects phenotype PMID:22491429
GO:0032740 Positive regulation of interleukin-17 production Affects phenotype PMID:22491429
GO:0032754 Positive regulation of interleukin-5 production Affects phenotype PMID:22491429
GO:0034440 Lipid oxidation Increases phenotype PMID:10647909
GO:0034753 Nuclear aryl hydrocarbon receptor complex Increases phenotype PMID:31225620
GO:0036211 Protein modification process Increases phenotype PMID:8386241
GO:0036296 Response to increased oxygen levels Increases phenotype PMID:28201809
GO:0040018 Positive regulation of multicellular organism growth Increases phenotype PMID:29180065
GO:0042157 Lipoprotein metabolic process Affects phenotype PMID:29521512
GO:0042178 Xenobiotic catabolic process Increases phenotype PMID:9817083; PMID:9817083; PMID:9929512; PMID:9929512
GO:0044237 Cellular metabolic process Decreases phenotype PMID:31756459; PMID:35124147; PMID:35124147
GO:0044238 Primary metabolic process Affects phenotype PMID:29521512
GO:0045541 Negative regulation of cholesterol biosynthetic process Affects phenotype PMID:22234961
GO:0045793 Positive regulation of cell size Increases phenotype PMID:19969063
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:27286660
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:15621696
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:29180065
GO:0048733 Sebaceous gland development Decreases phenotype PMID:28973660
GO:0060443 Mammary gland morphogenesis Decreases phenotype PMID:29521512
GO:0070989 Oxidative demethylation Increases phenotype PMID:22499231; PMID:22610983
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:25370011; PMID:25617484
GO:0090023 Positive regulation of neutrophil chemotaxis Increases phenotype PMID:29180065
GO:1900182 Positive regulation of protein localization to nucleus Increases phenotype PMID:29788535
GO:1901687 Glutathione derivative biosynthetic process Increases phenotype PMID:9429083
GO:1904654 Negative regulation of lung alveolus development Increases phenotype PMID:29180065
GO:2000321 Positive regulation of t-helper 17 cell differentiation Increases phenotype PMID:25716673

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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.