Octylphenol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:31566189
GO:0008284 Positive regulation of cell population proliferation Affects phenotype PMID:23810794
GO:0010942 Positive regulation of cell death Increases phenotype PMID:27825933
GO:0014064 Positive regulation of serotonin secretion Increases phenotype PMID:38642822
GO:0016049 Cell growth Decreases phenotype PMID:36277366
GO:0032869 Cellular response to insulin stimulus Decreases phenotype PMID:29935216
GO:0042593 Glucose homeostasis Affects phenotype PMID:29935216
GO:0044237 Cellular metabolic process Decreases phenotype PMID:36277366
GO:0045454 Cell redox homeostasis Decreases phenotype PMID:38642822
GO:0055070 Copper ion homeostasis Decreases phenotype PMID:27690074
GO:0055074 Calcium ion homeostasis Decreases phenotype PMID:27690074; PMID:29935216
GO:0060047 Heart contraction Decreases phenotype PMID:31566189
GO:0061526 Acetylcholine secretion Decreases phenotype PMID:38642822
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:38642822
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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.