N-Methyl-N-nitrosourea


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004784 Superoxide dismutase activity Increases phenotype PMID:39197506
GO:0006506 Gpi anchor biosynthetic process Decreases phenotype PMID:27931811
GO:0006749 Glutathione metabolic process Affects phenotype PMID:39197506
GO:0006915 Apoptotic process Increases phenotype PMID:10753191; PMID:24594278; PMID:28688903
GO:0006974 Cellular response to dna damage stimulus Affects phenotype PMID:27059372; PMID:27233451
GO:0008210 Estrogen metabolic process Affects phenotype PMID:39197506
GO:0008219 Cell death Increases phenotype PMID:30336191
GO:0008283 Cell population proliferation Affects phenotype PMID:24594278; PMID:35598691; PMID:38977090
GO:0022008 Neurogenesis Affects phenotype PMID:24463056
GO:0032125 Micronucleus organization Increases phenotype PMID:29110037; PMID:30944280
GO:0034440 Lipid oxidation Affects phenotype PMID:39197506
GO:0042221 Response to chemical Increases phenotype PMID:34428494
GO:0042448 Progesterone metabolic process Affects phenotype PMID:39197506
GO:0042756 Drinking behavior Affects phenotype PMID:38977090
GO:0043967 Histone h4 acetylation Decreases phenotype PMID:27233451
GO:0043981 Histone h4-k5 acetylation Decreases phenotype PMID:27233451
GO:0043982 Histone h4-k8 acetylation Decreases phenotype PMID:27233451
GO:0043983 Histone h4-k12 acetylation Decreases phenotype PMID:27233451
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:29110037
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:39197506
GO:2000252 Negative regulation of feeding behavior Increases phenotype PMID:38977090
GO:2000279 Negative regulation of dna biosynthetic process Decreases phenotype PMID:2909289
GO:2000619 Negative regulation of histone h4-k16 acetylation Increases phenotype PMID:27233451

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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.