Clotrimazole


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004743 Pyruvate kinase activity Decreases phenotype PMID:25863232
GO:0005227 Calcium activated cation channel activity Increases phenotype PMID:33872679
GO:0006006 Glucose metabolic process Decreases phenotype PMID:25863232
GO:0006695 Cholesterol biosynthetic process Decreases phenotype PMID:34890705
GO:0006749 Glutathione metabolic process Affects phenotype PMID:34890705
GO:0006754 Atp biosynthetic process Decreases phenotype PMID:25863232
GO:0006805 Xenobiotic metabolic process Decreases phenotype PMID:24021950
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:25863232
GO:0006915 Apoptotic process Increases phenotype PMID:10223459; PMID:12452064; PMID:20724915; PMID:24239969
GO:0007049 Cell cycle Decreases phenotype PMID:10223459; PMID:16121977; PMID:14985237; PMID:20724915
GO:0008283 Cell population proliferation Affects phenotype PMID:10223459; PMID:16121977; PMID:11129088; PMID:14985237; PMID:14985237; PMID:25863232; PMID:16121977; PMID:25863232; PMID:7585119
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:18694951
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:31330226; PMID:31549662
GO:0010942 Positive regulation of cell death Increases phenotype PMID:27507784
GO:0019722 Calcium-mediated signaling Affects phenotype PMID:11129088; PMID:14985237
GO:0022904 Respiratory electron transport chain Decreases phenotype PMID:25926417
GO:0030154 Cell differentiation Increases phenotype PMID:10223459; PMID:16121977
GO:0034440 Lipid oxidation Increases phenotype PMID:22033380
GO:0036438 Maintenance of lens transparency Affects phenotype PMID:34890705
GO:0042311 Vasodilation Increases phenotype PMID:11129088
GO:0042391 Regulation of membrane potential Increases phenotype PMID:14985237
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:22033380
GO:0044861 Protein transport into plasma membrane raft Increases phenotype PMID:22033380
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:22033380
GO:0045792 Negative regulation of cell size Increases phenotype PMID:22033380
GO:0046466 Membrane lipid catabolic process Decreases phenotype PMID:1884432
GO:0050810 Regulation of steroid biosynthetic process Affects phenotype PMID:26781511
GO:0051350 Negative regulation of lyase activity Increases phenotype PMID:31330226
GO:0090032 Negative regulation of steroid hormone biosynthetic process Increases phenotype PMID:31330226
GO:1900745 Positive regulation of p38mapk cascade Increases phenotype PMID:27507784
GO:1901381 Positive regulation of potassium ion transmembrane transport Increases phenotype PMID:33872679
GO:1901687 Glutathione derivative biosynthetic process Increases phenotype PMID:22033380
GO:1902043 Positive regulation of extrinsic apoptotic signaling pathway via death domain receptors Increases phenotype PMID:22033380
GO:1902046 Positive regulation of fas signaling pathway Increases phenotype PMID:22033380
GO:1903284 Positive regulation of glutathione peroxidase activity Decreases phenotype PMID:22033380
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:22033380
GO:1903766 Positive regulation of potassium ion export across plasma membrane Increases phenotype PMID:18187619
GO:2000304 Positive regulation of ceramide biosynthetic process Increases phenotype PMID:22033380
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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.