o-Cresyl phosphate


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000045 Autophagosome assembly Increases phenotype PMID:27267904; PMID:33617914
GO:0000423 Mitophagy Increases phenotype PMID:31100276
GO:0001541 Ovarian follicle development Decreases phenotype PMID:30439503
GO:0001780 Neutrophil homeostasis Affects phenotype PMID:29154782
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:26757727
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:26757727; PMID:27267904
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:26757727; PMID:27267904; PMID:31566301
GO:0006497 Protein lipidation Increases phenotype PMID:33617914
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:26757727; PMID:27267904
GO:0006914 Autophagy Increases phenotype PMID:25385720; PMID:27267904; PMID:33617914
GO:0006915 Apoptotic process Increases phenotype PMID:30439503
GO:0007005 Mitochondrion organization Decreases phenotype PMID:31100276; PMID:33617914
GO:0007033 Vacuole organization Increases phenotype PMID:29154782
GO:0007566 Embryo implantation Decreases phenotype PMID:31566301
GO:0008283 Cell population proliferation Decreases phenotype PMID:25385720; PMID:26757727; PMID:35503735
GO:0008344 Adult locomotory behavior Decreases phenotype PMID:29154782
GO:0008923 Lysine decarboxylase activity Decreases phenotype PMID:25264276
GO:0010942 Positive regulation of cell death Increases phenotype PMID:25199799
GO:0016042 Lipid catabolic process Increases phenotype PMID:26757727; PMID:27267904; PMID:31566301
GO:0016477 Cell migration Decreases phenotype PMID:33969458
GO:0030262 Apoptotic nuclear changes Increases phenotype PMID:11032765
GO:0031175 Neuron projection development Decreases phenotype PMID:33617914; PMID:33969458
GO:0032930 Positive regulation of superoxide anion generation Increases phenotype PMID:26794138
GO:0035265 Organ growth Decreases phenotype PMID:28321044
GO:0035702 Monocyte homeostasis Affects phenotype PMID:29154782
GO:0035936 Testosterone secretion Decreases phenotype PMID:27267904
GO:0035937 Estrogen secretion Increases phenotype PMID:30439503
GO:0042701 Progesterone secretion Decreases phenotype PMID:30439503
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:11032765
GO:0044237 Cellular metabolic process Decreases phenotype PMID:27267904; PMID:32234386; PMID:33617914; PMID:33969458
GO:0044295 Axonal growth cone Decreases phenotype PMID:38653376
GO:0048675 Axon extension Decreases phenotype PMID:31100276
GO:0048709 Oligodendrocyte differentiation Decreases phenotype PMID:33969458
GO:0050665 Hydrogen peroxide biosynthetic process Increases phenotype PMID:31566301
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:31100276; PMID:33617914
GO:0055074 Calcium ion homeostasis Affects phenotype PMID:30056177
GO:0060545 Positive regulation of necroptotic process Increases phenotype PMID:38653376
GO:0060711 Labyrinthine layer development Decreases phenotype PMID:31566301
GO:0060712 Spongiotrophoblast layer development Decreases phenotype PMID:31566301
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:33617914
GO:0072655 Establishment of protein localization to mitochondrion Affects phenotype PMID:31100276
GO:1903008 Organelle disassembly Increases phenotype PMID:25385720
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:31100276
GO:1990138 Neuron projection extension Decreases phenotype PMID:25199799
GO:1990266 Neutrophil migration Increases phenotype PMID:29154782
GO:2000872 Positive regulation of progesterone secretion Increases phenotype PMID:26794138
DISCLAIMER

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.