Procymidone


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:34503147
GO:0001544 Initiation of primordial ovarian follicle growth Increases phenotype PMID:34051340
GO:0006006 Glucose metabolic process Affects phenotype PMID:33246813; PMID:33246813; PMID:36764477; PMID:36764477
GO:0006090 Pyruvate metabolic process Affects phenotype PMID:33246813
GO:0006631 Fatty acid metabolic process Affects phenotype PMID:33246813
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:33246813; PMID:33246813; PMID:36764477; PMID:36764477
GO:0007283 Spermatogenesis Decreases phenotype PMID:35913088
GO:0008206 Bile acid metabolic process Affects phenotype PMID:36764477
GO:0008283 Cell population proliferation Increases phenotype PMID:33413771; PMID:34503147
GO:0009437 Carnitine metabolic process Affects phenotype PMID:33246813; PMID:33246813; PMID:36764477; PMID:36764477
GO:0034109 Homotypic cell-cell adhesion Increases phenotype PMID:34503147
GO:0036164 Cell-abiotic substrate adhesion Decreases phenotype PMID:34503147
GO:0040015 Negative regulation of multicellular organism growth Increases phenotype PMID:35913088
GO:0045333 Cellular respiration Increases phenotype PMID:34503147
GO:0046034 Atp metabolic process Affects phenotype PMID:34503147
GO:0048870 Cell motility Increases phenotype PMID:34503147
GO:0051091 Positive regulation of dna-binding transcription factor activity Increases phenotype PMID:28973306
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:33413771
GO:0097722 Sperm motility Decreases phenotype PMID:33413771
GO:2000844 Negative regulation of testosterone secretion Increases phenotype PMID:35913088
GO:2000848 Positive regulation of corticosteroid hormone secretion Increases phenotype PMID:34051340
GO:2000863 Positive regulation of estrogen secretion Increases phenotype PMID:34051340
GO:2000872 Positive regulation of progesterone secretion Increases phenotype PMID:34051340
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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.