Thiamethoxam


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:30520268
GO:0000755 Cytogamy Decreases phenotype PMID:33533595
GO:0001552 Ovarian follicle atresia Increases phenotype PMID:33533595
GO:0001556 Oocyte maturation Decreases phenotype PMID:33533595
GO:0001824 Blastocyst development Decreases phenotype PMID:29061322
GO:0001894 Tissue homeostasis Decreases phenotype PMID:30520268
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:29197058
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:29197058
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:29197058; PMID:30520268
GO:0004111 Creatine kinase activity Decreases phenotype PMID:30520268
GO:0004457 Lactate dehydrogenase activity Affects phenotype PMID:29197058; PMID:30520268
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:34181816; PMID:36958429
GO:0006590 Thyroid hormone generation Decreases phenotype PMID:31550567
GO:0006695 Cholesterol biosynthetic process Decreases phenotype PMID:29197058
GO:0006749 Glutathione metabolic process Increases phenotype PMID:30520268; PMID:34181816
GO:0006915 Apoptotic process Increases phenotype PMID:29197058; PMID:30621503; PMID:33533595
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:33533595
GO:0006979 Response to oxidative stress Increases phenotype PMID:30621503
GO:0007005 Mitochondrion organization Decreases phenotype PMID:33533595
GO:0008219 Cell death Increases phenotype PMID:29061322
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:30520268
GO:0008483 Transaminase activity Increases phenotype PMID:29197058
GO:0010940 Positive regulation of necrotic cell death Increases phenotype PMID:30520268
GO:0016042 Lipid catabolic process Increases phenotype PMID:30621503; PMID:34181816
GO:0018158 Protein oxidation Increases phenotype PMID:30520268
GO:0034440 Lipid oxidation Increases phenotype PMID:30520268; PMID:36958429
GO:0040015 Negative regulation of multicellular organism growth Increases phenotype PMID:31550567
GO:0040016 Embryonic cleavage Decreases phenotype PMID:29061322
GO:0042445 Hormone metabolic process Affects phenotype PMID:34073889
GO:0042632 Cholesterol homeostasis Decreases phenotype PMID:30520268
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:30520268
GO:0045123 Cellular extravasation Increases phenotype PMID:30621503
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:34181816
GO:0048311 Mitochondrion distribution Decreases phenotype PMID:33533595
GO:0051347 Positive regulation of transferase activity Increases phenotype PMID:30520268
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:33533595
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:34181816
GO:0070265 Necrotic cell death Increases phenotype PMID:30621503
GO:0070328 Triglyceride homeostasis Decreases phenotype PMID:30520268
GO:0070994 Detection of oxidative stress Increases phenotype PMID:36958429
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:33533595
GO:1903284 Positive regulation of glutathione peroxidase activity Increases phenotype PMID:30520268
GO:2000019 Negative regulation of male gonad development Decreases phenotype PMID:31550567
GO:2000195 Negative regulation of female gonad development Decreases phenotype PMID:31550567
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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.