Ethylbenzene


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001776 Leukocyte homeostasis Affects phenotype PMID:31988427
GO:0006749 Glutathione metabolic process Decreases phenotype PMID:21241565
GO:0007088 Regulation of mitotic nuclear division Decreases phenotype PMID:23138419
GO:0010424 Dna methylation on cytosine within a cg sequence Affects phenotype PMID:33438815
GO:0030097 Hemopoiesis Affects phenotype PMID:31988427
GO:0030220 Platelet formation Affects phenotype PMID:31988427
GO:0032286 Central nervous system myelin maintenance Decreases phenotype PMID:21241565
GO:0034440 Lipid oxidation Increases phenotype PMID:21241565; PMID:25518993
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:21241565; PMID:25518993
GO:0055075 Potassium ion homeostasis Affects phenotype PMID:33722544
GO:1901671 Positive regulation of superoxide dismutase activity Decreases phenotype PMID:24053957; PMID:25518993
GO:1903284 Positive regulation of glutathione peroxidase activity Decreases phenotype PMID:24053957; PMID:25518993

DISCLAIMER

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.