Phtpp


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000266 Mitochondrial fission Affects phenotype PMID:34023961
GO:0001525 Angiogenesis Increases phenotype PMID:35051763
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:27581038
GO:0004722 Protein serine/threonine phosphatase activity Increases phenotype PMID:34023961
GO:0005248 Voltage-gated sodium channel activity Increases phenotype PMID:31312012
GO:0006626 Protein targeting to mitochondrion Affects phenotype PMID:34023961
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:34023961
GO:0006915 Apoptotic process Increases phenotype PMID:35461094
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:29307715
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:31381935
GO:0014808 Release of sequestered calcium ion into cytosol by sarcoplasmic reticulum Increases phenotype PMID:25723814
GO:0016477 Cell migration Increases phenotype PMID:35007301
GO:0030199 Collagen fibril organization Increases phenotype PMID:35051763
GO:0030282 Bone mineralization Increases phenotype PMID:29428397
GO:0036446 Myofibroblast differentiation Increases phenotype PMID:35051763
GO:0044237 Cellular metabolic process Affects phenotype PMID:30552153; PMID:34602561
GO:0045880 Positive regulation of smoothened signaling pathway Increases phenotype PMID:29307715
GO:0048699 Generation of neurons Increases phenotype PMID:29425760
GO:0070374 Positive regulation of erk1 and erk2 cascade Increases phenotype PMID:27071941
GO:0086003 Cardiac muscle cell contraction Increases phenotype PMID:25723814
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:30088793
GO:2000866 Positive regulation of estradiol secretion Increases phenotype PMID:37717640
GO:2000872 Positive regulation of progesterone secretion Increases phenotype PMID:37717640
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.