Chlordecone


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000711 Meiotic dna repair synthesis Affects phenotype PMID:29980752
GO:0001552 Ovarian follicle atresia Increases phenotype PMID:31084621
GO:0006304 Dna modification Increases phenotype PMID:31084621
GO:0007283 Spermatogenesis Affects phenotype PMID:29980752
GO:0008283 Cell population proliferation Decreases phenotype PMID:17599374
GO:0010467 Gene expression Affects phenotype PMID:29980752
GO:0035518 Histone h2a monoubiquitination Increases phenotype PMID:31084621
GO:0036124 Histone h3-k9 trimethylation Decreases phenotype PMID:33837044
GO:0040015 Negative regulation of multicellular organism growth Increases phenotype PMID:31084621
GO:0040029 Epigenetic regulation of gene expression Affects phenotype PMID:29980752
GO:0043967 Histone h4 acetylation Decreases phenotype PMID:33711761
GO:0043981 Histone h4-k5 acetylation Affects phenotype PMID:29980752
GO:0045931 Positive regulation of mitotic cell cycle Increases phenotype PMID:35307500
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:31084621
GO:0051321 Meiotic cell cycle Affects phenotype PMID:29980752
GO:0060009 Sertoli cell development Affects phenotype PMID:29980752
GO:0080182 Histone h3-k4 trimethylation Decreases phenotype PMID:29980752; PMID:31084621; PMID:33711761; PMID:33837044
GO:0090241 Negative regulation of histone h4 acetylation Increases phenotype PMID:31084621
GO:0098532 Histone h3-k27 trimethylation Decreases phenotype PMID:33711761
GO:1902466 Positive regulation of histone h3-k27 trimethylation Increases phenotype PMID:31084621
GO:1904356 Regulation of telomere maintenance via telomere lengthening Affects phenotype PMID:33837044
GO:1905132 Regulation of meiotic chromosome separation Affects phenotype PMID:29980752
GO:1990918 Double-strand break repair involved in meiotic recombination Decreases phenotype PMID:31084621
GO:2000355 Negative regulation of ovarian follicle development Increases phenotype PMID:31084621
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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.