Methyl parathion


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:20100039
GO:0004104 Cholinesterase activity Decreases phenotype PMID:30035273
GO:0004602 Glutathione peroxidase activity Affects phenotype PMID:20100039; PMID:29319433
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:20100039
GO:0006094 Gluconeogenesis Increases phenotype PMID:29319433
GO:0006304 Dna modification Increases phenotype PMID:27941166
GO:0006325 Chromatin organization Decreases phenotype PMID:32294493
GO:0006601 Creatine biosynthetic process Increases phenotype PMID:29319433
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:29319433
GO:0007213 G protein-coupled acetylcholine receptor signaling pathway Increases phenotype PMID:11750078
GO:0007286 Spermatid development Decreases phenotype PMID:32294493
GO:0010669 Epithelial structure maintenance Decreases phenotype PMID:32294493
GO:0010942 Positive regulation of cell death Increases phenotype PMID:26688254; PMID:32294493
GO:0018158 Protein oxidation Increases phenotype PMID:29540303; PMID:32294493
GO:0018198 Peptidyl-cysteine modification Increases phenotype PMID:22271348
GO:0034440 Lipid oxidation Increases phenotype PMID:27941166; PMID:32294493
GO:0035811 Negative regulation of urine volume Increases phenotype PMID:29319433
GO:0036374 Glutathione hydrolase activity Increases phenotype PMID:29319433
GO:0044090 Positive regulation of vacuole organization Increases phenotype PMID:26688254
GO:0045919 Positive regulation of cytolysis Increases phenotype PMID:27941166
GO:0070633 Transepithelial transport Decreases phenotype PMID:32294493
GO:0090116 C-5 methylation of cytosine Decreases phenotype PMID:29540303
GO:1901318 Negative regulation of flagellated sperm motility Increases phenotype PMID:32294493
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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.