Myricetin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:35156864
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:35156864
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:35156864
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:35156864
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:35156864
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:35156864
GO:0004791 Thioredoxin-disulfide reductase activity Affects phenotype PMID:16618767
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:29698783
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:35156864
GO:0006695 Cholesterol biosynthetic process Increases phenotype PMID:25240712
GO:0006749 Glutathione metabolic process Affects phenotype PMID:35156864
GO:0006750 Glutathione biosynthetic process Increases phenotype PMID:9920463
GO:0006874 Cellular calcium ion homeostasis Affects phenotype PMID:33276066
GO:0006915 Apoptotic process Increases phenotype PMID:29698783; PMID:39581298
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:32107588; PMID:32342131
GO:0006979 Response to oxidative stress Increases phenotype PMID:15904944
GO:0008203 Cholesterol metabolic process Affects phenotype PMID:35156864
GO:0008219 Cell death Increases phenotype PMID:16618767
GO:0008283 Cell population proliferation Affects phenotype PMID:18946510
GO:0008654 Phospholipid biosynthetic process Increases phenotype PMID:25240712
GO:0010942 Positive regulation of cell death Decreases phenotype PMID:22683914
GO:0015705 Iodide transport Affects phenotype PMID:39581298
GO:0016042 Lipid catabolic process Increases phenotype PMID:35156864
GO:0016049 Cell growth Decreases phenotype PMID:29698783
GO:0016887 Atp hydrolysis activity Increases phenotype PMID:34217736
GO:0019432 Triglyceride biosynthetic process Increases phenotype PMID:25240712
GO:0032125 Micronucleus organization Affects phenotype PMID:32220605; PMID:32342131
GO:0034614 Cellular response to reactive oxygen species Decreases phenotype PMID:22683914
GO:0035847 Uterine epithelium development Increases phenotype PMID:24487097
GO:0042158 Lipoprotein biosynthetic process Affects phenotype PMID:25240712
GO:0044237 Cellular metabolic process Decreases phenotype PMID:33276066; PMID:39581298
GO:0044319 Wound healing, spreading of cells Increases phenotype PMID:29698783
GO:0045333 Cellular respiration Decreases phenotype PMID:36116563
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:16618767
GO:0045944 Positive regulation of transcription by rna polymerase ii Increases phenotype PMID:28668616
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:35156864
GO:0046326 Positive regulation of glucose import Decreases phenotype PMID:25719685
GO:0050766 Positive regulation of phagocytosis Decreases phenotype PMID:17958546
GO:0051092 Positive regulation of nf-kappab transcription factor activity Decreases phenotype PMID:22683914
GO:0061951 Establishment of protein localization to plasma membrane Increases phenotype PMID:30591588
GO:0070265 Necrotic cell death Increases phenotype PMID:35156864
GO:0070633 Transepithelial transport Increases phenotype PMID:33276066
GO:1900745 Positive regulation of p38mapk cascade Decreases phenotype PMID:22683914
GO:1901224 Positive regulation of nik/nf-kappab signaling Decreases phenotype PMID:22683914
GO:1903409 Reactive oxygen species biosynthetic process Decreases phenotype PMID:19958256
GO:1903709 Uterine gland development Increases phenotype PMID:24487097
GO:2001038 Regulation of cellular response to drug Affects phenotype PMID:38401715
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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.