Cyfluthrin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000084 Mitotic s phase Affects phenotype PMID:35126122
GO:0000086 G2/m transition of mitotic cell cycle Affects phenotype PMID:35126122
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:35126122
GO:0001890 Placenta development Affects phenotype PMID:36548566
GO:0001944 Vasculature development Affects phenotype PMID:36548566
GO:0004017 Adenylate kinase activity Affects phenotype PMID:32028016
GO:0004035 Alkaline phosphatase activity Affects phenotype PMID:35126122
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Affects phenotype PMID:35126122
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:35126122
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:35126122
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:35126122
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:35126122
GO:0006749 Glutathione metabolic process Affects phenotype PMID:35126122
GO:0006816 Calcium ion transport Affects phenotype PMID:32314600
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:32314600
GO:0007009 Plasma membrane organization Decreases phenotype PMID:32028016
GO:0007566 Embryo implantation Affects phenotype PMID:36548566
GO:0008283 Cell population proliferation Decreases phenotype PMID:36548566
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:31330490
GO:0010508 Positive regulation of autophagy Increases phenotype PMID:36515635
GO:0018158 Protein oxidation Increases phenotype PMID:35126122
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:36548566
GO:0030336 Negative regulation of cell migration Increases phenotype PMID:36515635
GO:0033148 Positive regulation of intracellular estrogen receptor signaling pathway Increases phenotype PMID:25449125
GO:0034440 Lipid oxidation Increases phenotype PMID:23595963; PMID:31330490; PMID:35126122; PMID:36515635
GO:0042178 Xenobiotic catabolic process Increases phenotype PMID:23639246
GO:0042743 Hydrogen peroxide metabolic process Affects phenotype PMID:35126122
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32028016; PMID:32314600
GO:0045023 G0 to g1 transition Affects phenotype PMID:35126122
GO:0045429 Positive regulation of nitric oxide biosynthetic process Increases phenotype PMID:31330490
GO:0045919 Positive regulation of cytolysis Increases phenotype PMID:36515635
GO:0061739 Protein lipidation involved in autophagosome assembly Increases phenotype PMID:36515635
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:32028016
GO:0097189 Apoptotic body Increases phenotype PMID:36548566
GO:0097202 Activation of cysteine-type endopeptidase activity Increases phenotype PMID:32028016
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:36515635
GO:1901671 Positive regulation of superoxide dismutase activity Decreases phenotype PMID:23595963
GO:1903047 Mitotic cell cycle process Affects phenotype PMID:35126122
GO:1903284 Positive regulation of glutathione peroxidase activity Decreases phenotype PMID:23595963
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:31330490; PMID:36515635
GO:1905605 Positive regulation of blood-brain barrier permeability Increases phenotype PMID:36167171
GO:1990962 Xenobiotic transport across blood-brain barrier Increases phenotype PMID:36167171
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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.