Tri-(2-chloroisopropyl)phosphate


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000266 Mitochondrial fission Affects phenotype PMID:36115506
GO:0001958 Endochondral ossification Decreases phenotype PMID:33367866
GO:0002924 Negative regulation of humoral immune response mediated by circulating immunoglobulin Decreases phenotype PMID:39908456
GO:0005739 Mitochondrion Increases phenotype PMID:38518089
GO:0005764 Lysosome Increases phenotype PMID:38518089
GO:0007040 Lysosome organization Increases phenotype PMID:35135005
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:33641188
GO:0008361 Regulation of cell size Affects phenotype PMID:29945461
GO:0008923 Lysine decarboxylase activity Decreases phenotype PMID:25264276
GO:0019637 Organophosphate metabolic process Affects phenotype PMID:38734222
GO:0042098 T cell proliferation Affects phenotype PMID:39908456
GO:0042701 Progesterone secretion Affects phenotype PMID:36115506
GO:0043299 Leukocyte degranulation Affects phenotype PMID:29945461
GO:0044237 Cellular metabolic process Decreases phenotype PMID:29945461; PMID:36115506
GO:0046034 Atp metabolic process Affects phenotype PMID:36115506
GO:0051882 Mitochondrial depolarization Increases phenotype PMID:33641188; PMID:36115506
GO:0070265 Necrotic cell death Increases phenotype PMID:29945461
GO:0070328 Triglyceride homeostasis Decreases phenotype PMID:30966736
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:36115506; PMID:38518089
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:33641188; PMID:35135005; PMID:38603619
GO:2000003 Positive regulation of dna damage checkpoint Increases phenotype PMID:33641188
GO:2000866 Positive regulation of estradiol secretion Increases phenotype PMID:38603619
GO:2000872 Positive regulation of progesterone secretion Increases phenotype PMID:38603619
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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.