Catechol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006915 Apoptotic process Increases phenotype PMID:23776099
GO:0008283 Cell population proliferation Decreases phenotype PMID:23776099; PMID:23776099; PMID:24141029; PMID:24141029
GO:0008284 Positive regulation of cell population proliferation Affects phenotype PMID:23535288
GO:0010424 Dna methylation on cytosine within a cg sequence Affects phenotype PMID:28552822
GO:0015732 Prostaglandin transport Increases phenotype PMID:34681798
GO:0030218 Erythrocyte differentiation Increases phenotype PMID:24141029
GO:0034116 Positive regulation of heterotypic cell-cell adhesion Increases phenotype PMID:34718823
GO:0034440 Lipid oxidation Increases phenotype PMID:106178
GO:0042541 Hemoglobin biosynthetic process Increases phenotype PMID:24141029
GO:0044030 Regulation of dna methylation Affects phenotype PMID:28552822
GO:0045648 Positive regulation of erythrocyte differentiation Increases phenotype PMID:28552822
GO:0046985 Positive regulation of hemoglobin biosynthetic process Increases phenotype PMID:28552822
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:23776099
GO:0070268 Cornification Increases phenotype PMID:38598786
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:23776099
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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.