Ethambutol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0002253 Activation of immune response Increases phenotype PMID:27933861
GO:0003939 L-iditol 2-dehydrogenase activity Decreases phenotype PMID:34118364
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:34118364
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:34118364
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:27919644; PMID:36878459
GO:0006089 Lactate metabolic process Increases phenotype PMID:34118364
GO:0006749 Glutathione metabolic process Increases phenotype PMID:27334974; PMID:34118364; PMID:36878459
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:27919644
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:27919644
GO:0007283 Spermatogenesis Decreases phenotype PMID:27334974; PMID:27919644; PMID:34118364
GO:0008206 Bile acid metabolic process Affects phenotype PMID:35835356
GO:0010693 Negative regulation of alkaline phosphatase activity Increases phenotype PMID:34118364
GO:0010942 Positive regulation of cell death Increases phenotype PMID:34118364
GO:0016042 Lipid catabolic process Increases phenotype PMID:27919644
GO:0034418 Urate biosynthetic process Increases phenotype PMID:34118364
GO:0034440 Lipid oxidation Increases phenotype PMID:27334974; PMID:34118364; PMID:36878459
GO:0042104 Positive regulation of activated t cell proliferation Increases phenotype PMID:27933861
GO:0043372 Positive regulation of cd4-positive, alpha-beta t cell differentiation Increases phenotype PMID:27933861
GO:0043378 Positive regulation of cd8-positive, alpha-beta t cell differentiation Increases phenotype PMID:27933861
GO:0044237 Cellular metabolic process Decreases phenotype PMID:35835356; PMID:36878459
GO:0045429 Positive regulation of nitric oxide biosynthetic process Increases phenotype PMID:34118364
GO:0045930 Negative regulation of mitotic cell cycle Affects phenotype PMID:27919644
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:34118364
GO:0050878 Regulation of body fluid levels Decreases phenotype PMID:34118364
GO:0051347 Positive regulation of transferase activity Increases phenotype PMID:34118364
GO:0051348 Negative regulation of transferase activity Affects phenotype PMID:34118364
GO:0051353 Positive regulation of oxidoreductase activity Increases phenotype PMID:34118364
GO:0051354 Negative regulation of oxidoreductase activity Affects phenotype PMID:34118364
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:36878459
GO:0055072 Iron ion homeostasis Affects phenotype PMID:36878459
GO:0070265 Necrotic cell death Increases phenotype PMID:36878459
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:36878459
GO:0098727 Maintenance of cell number Decreases phenotype PMID:34118364
GO:0110111 Negative regulation of animal organ morphogenesis Increases phenotype PMID:34118364
GO:0140042 Lipid droplet formation Increases phenotype PMID:35835356; PMID:36878459
GO:1901318 Negative regulation of flagellated sperm motility Increases phenotype PMID:34118364
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:34118364
GO:1902512 Positive regulation of apoptotic dna fragmentation Increases phenotype PMID:27334974
GO:1903283 Negative regulation of glutathione peroxidase activity Increases phenotype PMID:34118364
GO:2000844 Negative regulation of testosterone secretion Increases phenotype PMID:27334974
GO:2001025 Positive regulation of response to drug Increases phenotype PMID:34118364
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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.