Parathion


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001964 Startle response Decreases phenotype PMID:18817854
GO:0002638 Negative regulation of immunoglobulin production Increases phenotype PMID:24188624
GO:0002639 Positive regulation of immunoglobulin production Increases phenotype PMID:24935097
GO:0004064 Arylesterase activity Increases phenotype PMID:36058312
GO:0006749 Glutathione metabolic process Increases phenotype PMID:34778934; PMID:36058312
GO:0007193 Adenylate cyclase-inhibiting g protein-coupled receptor signaling pathway Increases phenotype PMID:20074626
GO:0007197 Adenylate cyclase-inhibiting g protein-coupled acetylcholine receptor signaling pathway Increases phenotype PMID:20074626
GO:0007208 Phospholipase c-activating serotonin receptor signaling pathway Increases phenotype PMID:18773955; PMID:19616088; PMID:20015457
GO:0007213 G protein-coupled acetylcholine receptor signaling pathway Decreases phenotype PMID:17707571
GO:0007283 Spermatogenesis Affects phenotype PMID:17375462
GO:0007611 Learning or memory Increases phenotype PMID:18817854
GO:0008283 Cell population proliferation Affects phenotype PMID:11401758; PMID:28174098; PMID:34813904
GO:0010701 Positive regulation of norepinephrine secretion Increases phenotype PMID:10685507
GO:0010942 Positive regulation of cell death Increases phenotype PMID:26196221
GO:0030187 Melatonin biosynthetic process Increases phenotype PMID:10685507
GO:0031324 Negative regulation of cellular metabolic process Increases phenotype PMID:36058312
GO:0032148 Activation of protein kinase b activity Decreases phenotype PMID:36058312
GO:0032812 Positive regulation of epinephrine secretion Increases phenotype PMID:10685507
GO:0035641 Locomotory exploration behavior Increases phenotype PMID:18817854
GO:0042417 Dopamine metabolic process Increases phenotype PMID:19616088
GO:0042428 Serotonin metabolic process Increases phenotype PMID:10685507; PMID:19616088
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:11032765; PMID:11032765; PMID:36058312; PMID:36458919
GO:0045444 Fat cell differentiation Affects phenotype PMID:28174098
GO:0045687 Positive regulation of glial cell differentiation Decreases phenotype PMID:27816694
GO:0045762 Positive regulation of adenylate cyclase activity Increases phenotype PMID:20074626
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:36458919
GO:0051092 Positive regulation of nf-kappab transcription factor activity Increases phenotype PMID:30978295
GO:0051345 Positive regulation of hydrolase activity Increases phenotype PMID:36058312
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:36458919
GO:0060408 Regulation of acetylcholine metabolic process Affects phenotype PMID:17707571
GO:0061744 Motor behavior Decreases phenotype PMID:17707571
GO:0071879 Positive regulation of adenylate cyclase-activating adrenergic receptor signaling pathway Affects phenotype PMID:20074626
GO:0090326 Positive regulation of locomotion involved in locomotory behavior Affects phenotype PMID:17707571; PMID:18817854
GO:0095500 Acetylcholine receptor signaling pathway Increases phenotype PMID:18941570; PMID:20015457
GO:0098751 Bone cell development Affects phenotype PMID:28174098
GO:1900017 Positive regulation of cytokine production involved in inflammatory response Increases phenotype PMID:24935097
GO:1901569 Fatty acid derivative catabolic process Decreases phenotype PMID:26215119
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:36458919
GO:2001025 Positive regulation of response to drug Decreases phenotype PMID:18817854
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.