Phloretin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000084 Mitotic s phase Affects phenotype PMID:34896434
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:35547012; PMID:39177155
GO:0004096 Catalase activity Increases phenotype PMID:39177155
GO:0004364 Glutathione transferase activity Affects phenotype PMID:33410021; PMID:39177155
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:30287234
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:33410021; PMID:35547012; PMID:39177155
GO:0006338 Chromatin remodeling Increases phenotype PMID:34896434
GO:0006606 Protein import into nucleus Affects phenotype PMID:34037972
GO:0006749 Glutathione metabolic process Affects phenotype PMID:33410021; PMID:34896434; PMID:35547012; PMID:39177155
GO:0006833 Water transport Affects phenotype PMID:9733774
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:34037972
GO:0006915 Apoptotic process Affects phenotype PMID:34037972; PMID:34896434; PMID:39059605
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:33410021
GO:0008283 Cell population proliferation Affects phenotype PMID:22770624
GO:0009636 Response to toxic substance Decreases phenotype PMID:29566083
GO:0010884 Positive regulation of lipid storage Increases phenotype PMID:39793953
GO:0016042 Lipid catabolic process Affects phenotype PMID:33410021
GO:0016049 Cell growth Decreases phenotype PMID:30287234
GO:0018158 Protein oxidation Increases phenotype PMID:33410021; PMID:39177155
GO:0034440 Lipid oxidation Affects phenotype PMID:24613711; PMID:35547012; PMID:39177155
GO:0035435 Phosphate ion transmembrane transport Increases phenotype PMID:12672655
GO:0036211 Protein modification process Increases phenotype PMID:35547012
GO:0044237 Cellular metabolic process Decreases phenotype PMID:26633321; PMID:34896434; PMID:39059605
GO:0045023 G0 to g1 transition Affects phenotype PMID:34896434
GO:0045722 Positive regulation of gluconeogenesis Decreases phenotype PMID:35872042
GO:0045819 Positive regulation of glycogen catabolic process Decreases phenotype PMID:35872042
GO:0046323 Glucose import Decreases phenotype PMID:31618665
GO:0046326 Positive regulation of glucose import Decreases phenotype PMID:26616219
GO:0046961 Proton-transporting atpase activity, rotational mechanism Decreases phenotype PMID:10882397
GO:0061621 Canonical glycolysis Increases phenotype PMID:35872042
GO:0070265 Necrotic cell death Increases phenotype PMID:39177155
GO:0070327 Thyroid hormone transport Decreases phenotype PMID:28119167
GO:0071243 Cellular response to arsenic-containing substance Affects phenotype PMID:35547012
GO:0071247 Cellular response to chromate Affects phenotype PMID:35547012
GO:0071674 Mononuclear cell migration Increases phenotype PMID:39177155
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:32408695; PMID:39059605
GO:0072756 Cellular response to paraquat Affects phenotype PMID:39059605
GO:0097722 Sperm motility Decreases phenotype PMID:33410021
GO:1901216 Positive regulation of neuron death Increases phenotype PMID:29566083
GO:1903047 Mitotic cell cycle process Affects phenotype PMID:34896434
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:22770624
GO:1903709 Uterine gland development Increases phenotype PMID:24487097
GO:2001170 Negative regulation of atp biosynthetic process Increases phenotype PMID:35872042
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.