Carbaryl


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006306 Dna methylation Increases phenotype PMID:33865946
GO:0006701 Progesterone biosynthetic process Decreases phenotype PMID:27665777
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:27214522
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:26187449
GO:0006915 Apoptotic process Affects phenotype PMID:27296064; PMID:27829164
GO:0006997 Nucleus organization Decreases phenotype PMID:27296064
GO:0007596 Blood coagulation Decreases phenotype PMID:27214522
GO:0008283 Cell population proliferation Decreases phenotype PMID:27214522; PMID:27829164
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:32949729
GO:0010942 Positive regulation of cell death Increases phenotype PMID:20654549
GO:0019226 Transmission of nerve impulse Decreases phenotype PMID:38599286
GO:0022602 Ovulation cycle process Affects phenotype PMID:27665777
GO:0030220 Platelet formation Decreases phenotype PMID:27214522
GO:0044849 Estrous cycle Decreases phenotype PMID:27665777
GO:0046034 Atp metabolic process Affects phenotype PMID:32949729
GO:0051091 Positive regulation of dna-binding transcription factor activity Increases phenotype PMID:28973306
GO:1901386 Negative regulation of voltage-gated calcium channel activity Increases phenotype PMID:26187449

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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.