Mitomycin C


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000086 G2/m transition of mitotic cell cycle Increases phenotype PMID:32087850
GO:0000165 Mapk cascade Increases phenotype PMID:20002897
GO:0000278 Mitotic cell cycle Decreases phenotype PMID:1901354; PMID:2568944
GO:0000281 Mitotic cytokinesis Decreases phenotype PMID:30103639
GO:0000723 Telomere maintenance Affects phenotype PMID:24838295
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:35882637
GO:0006308 Dna catabolic process Increases phenotype PMID:34196753
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:10960761; PMID:16186332; PMID:17094455; PMID:19834285
GO:0006606 Protein import into nucleus Increases phenotype PMID:35882637
GO:0006754 Atp biosynthetic process Affects phenotype PMID:35435491
GO:0006915 Apoptotic process Affects phenotype PMID:10960761; PMID:9815832; PMID:11392669; PMID:15905168; PMID:11867586; PMID:16186332; PMID:9478007; PMID:12181741; PMID:12181741; PMID:9815832; PMID:15905168; PMID:16019139; PMID:17021654; PMID:16186332; PMID:17021654; PMID:17530733; PMID:19834285; PMID:17641843; PMID:18304466; PMID:18615204; PMID:20002897; PMID:19834285; PMID:24838295; PMID:9815832
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:24838295
GO:0006979 Response to oxidative stress Increases phenotype PMID:16226770
GO:0007049 Cell cycle Decreases phenotype PMID:2492079
GO:0008219 Cell death Increases phenotype PMID:16113371; PMID:16226770; PMID:16585851; PMID:1701346; PMID:17094455; PMID:28007550; PMID:28531190
GO:0008283 Cell population proliferation Affects phenotype PMID:16585851; PMID:19255723; PMID:20002897; PMID:24838295; PMID:8701039
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:25275039
GO:0008285 Negative regulation of cell population proliferation Affects phenotype PMID:28535027; PMID:31563593; PMID:32197950; PMID:34196753
GO:0010942 Positive regulation of cell death Increases phenotype PMID:25772433; PMID:28077981
GO:0032125 Micronucleus organization Increases phenotype PMID:18621143; PMID:26542539; PMID:29502740; PMID:35321623; PMID:30944280; PMID:32050487; PMID:32087850; PMID:32220605; PMID:32512035; PMID:35882637
GO:0034088 Maintenance of mitotic sister chromatid cohesion Affects phenotype PMID:34334017
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:28126644
GO:0044237 Cellular metabolic process Decreases phenotype PMID:26178874; PMID:28531190; PMID:28531190; PMID:35321623; PMID:32087850
GO:0045793 Positive regulation of cell size Increases phenotype PMID:20002897
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:29703973; PMID:32087850
GO:0045951 Positive regulation of mitotic recombination Increases phenotype PMID:28077981
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:6411900
GO:0051881 Regulation of mitochondrial membrane potential Decreases phenotype PMID:16186332; PMID:19834285
GO:0061739 Protein lipidation involved in autophagosome assembly Increases phenotype PMID:31563593
GO:0070987 Error-free translesion synthesis Increases phenotype PMID:28077981
GO:0090116 C-5 methylation of cytosine Decreases phenotype PMID:27032448
GO:0090398 Cellular senescence Increases phenotype PMID:34624459
GO:0097237 Cellular response to toxic substance Affects phenotype PMID:29502735
GO:0120187 Positive regulation of protein localization to chromatin Increases phenotype PMID:28535027
GO:1902520 Response to doxorubicin Decreases phenotype PMID:31563593
GO:1902527 Positive regulation of protein monoubiquitination Increases phenotype PMID:28535027
GO:1990414 Replication-born double-strand break repair via sister chromatid exchange Increases phenotype PMID:34334017; PMID:6409956
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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.