Phenanthrene


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0003993 Acid phosphatase activity Increases phenotype PMID:28710019
GO:0004784 Superoxide dismutase activity Increases phenotype PMID:31456356; PMID:32856796
GO:0005243 Gap junction channel activity Decreases phenotype PMID:26023933
GO:0006749 Glutathione metabolic process Increases phenotype PMID:29526570; PMID:31181217; PMID:34453960
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:31456356
GO:0007033 Vacuole organization Increases phenotype PMID:31456356
GO:0007204 Positive regulation of cytosolic calcium ion concentration Increases phenotype PMID:20238386
GO:0008219 Cell death Increases phenotype PMID:29502740
GO:0008283 Cell population proliferation Increases phenotype PMID:28710019
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:29526570
GO:0010729 Positive regulation of hydrogen peroxide biosynthetic process Increases phenotype PMID:20238386
GO:0010940 Positive regulation of necrotic cell death Increases phenotype PMID:31181217
GO:0010942 Positive regulation of cell death Increases phenotype PMID:20238386
GO:0016042 Lipid catabolic process Increases phenotype PMID:31456356; PMID:32856796
GO:0018158 Protein oxidation Decreases phenotype PMID:20238386
GO:0021766 Hippocampus development Affects phenotype PMID:34453960
GO:0031325 Positive regulation of cellular metabolic process Increases phenotype PMID:28803881
GO:0032125 Micronucleus organization Increases phenotype PMID:29502740
GO:0032930 Positive regulation of superoxide anion generation Increases phenotype PMID:20238386
GO:0034440 Lipid oxidation Increases phenotype PMID:20238386
GO:0035176 Social behavior Decreases phenotype PMID:34453960
GO:0035640 Exploration behavior Decreases phenotype PMID:34453960
GO:0043433 Negative regulation of dna-binding transcription factor activity Increases phenotype PMID:26022396
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32856796; PMID:33359405
GO:0045429 Positive regulation of nitric oxide biosynthetic process Increases phenotype PMID:20238386
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:20238386
GO:0050765 Negative regulation of phagocytosis Increases phenotype PMID:20238386
GO:0050847 Progesterone receptor signaling pathway Decreases phenotype PMID:26022396
GO:0070959 Negative regulation of neutrophil mediated killing of fungus Increases phenotype PMID:20238386
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:12730081; PMID:32856796; PMID:34453960
GO:1900119 Positive regulation of execution phase of apoptosis Increases phenotype PMID:29526570
GO:1900182 Positive regulation of protein localization to nucleus Increases phenotype PMID:31181217
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:29526570
GO:1901671 Positive regulation of superoxide dismutase activity Increases phenotype PMID:20238386
GO:1903284 Positive regulation of glutathione peroxidase activity Increases phenotype PMID:20238386
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:29526570
GO:1990266 Neutrophil migration Increases phenotype PMID:31456356
GO:2000865 Negative regulation of estradiol secretion Increases phenotype PMID:28803881
GO:2000871 Negative regulation of progesterone secretion Increases phenotype PMID:28803881
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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.