Chrysin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001516 Prostaglandin biosynthetic process Increases phenotype PMID:24134915
GO:0001808 Negative regulation of type iv hypersensitivity Increases phenotype PMID:36114367
GO:0001913 T cell mediated cytotoxicity Increases phenotype PMID:29352974
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:30974023
GO:0002921 Negative regulation of humoral immune response Increases phenotype PMID:36114367
GO:0003016 Respiratory system process Decreases phenotype PMID:30974023
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:28682524; PMID:31625388
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:28682524; PMID:31625388
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:28682524; PMID:33121995
GO:0004697 Protein kinase c activity Affects phenotype PMID:32220030
GO:0004784 Superoxide dismutase activity Affects phenotype PMID:28682524; PMID:29247772; PMID:32220030; PMID:33121995; PMID:34774662
GO:0006182 Cgmp biosynthetic process Decreases phenotype PMID:37263553
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:20457140
GO:0006641 Triglyceride metabolic process Affects phenotype PMID:32220030
GO:0006695 Cholesterol biosynthetic process Increases phenotype PMID:25169908
GO:0006749 Glutathione metabolic process Increases phenotype PMID:30273961; PMID:30500344
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:28458011; PMID:28682524; PMID:29247772; PMID:30974023
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:24932515; PMID:29352974; PMID:30974023
GO:0006915 Apoptotic process Increases phenotype PMID:20457140; PMID:25770930; PMID:26367700; PMID:26408079; PMID:29352974
GO:0006954 Inflammatory response Increases phenotype PMID:32220030
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:29308674
GO:0007049 Cell cycle Decreases phenotype PMID:20457140
GO:0007283 Spermatogenesis Decreases phenotype PMID:24932515
GO:0007613 Memory Affects phenotype PMID:34774662
GO:0008219 Cell death Increases phenotype PMID:18455702; PMID:25770930; PMID:28458011
GO:0008283 Cell population proliferation Affects phenotype PMID:24213142; PMID:25058688; PMID:26367700
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:35779630
GO:0010942 Positive regulation of cell death Increases phenotype PMID:30273961
GO:0016042 Lipid catabolic process Increases phenotype PMID:28682524; PMID:29247772; PMID:29308674; PMID:30974023; PMID:32220030; PMID:34774662
GO:0016049 Cell growth Decreases phenotype PMID:29352974
GO:0016477 Cell migration Affects phenotype PMID:24122885; PMID:26408079; PMID:30016632
GO:0018158 Protein oxidation Increases phenotype PMID:29308674; PMID:34774662
GO:0030101 Natural killer cell activation Increases phenotype PMID:29352974
GO:0030154 Cell differentiation Increases phenotype PMID:20457140
GO:0030218 Erythrocyte differentiation Increases phenotype PMID:25058688
GO:0031987 Locomotion involved in locomotory behavior Increases phenotype PMID:29054324
GO:0032125 Micronucleus organization Increases phenotype PMID:29308674
GO:0033212 Iron import into cell Increases phenotype PMID:38432408
GO:0034197 Triglyceride transport Affects phenotype PMID:32220030
GO:0034361 Very-low-density lipoprotein particle Affects phenotype PMID:32220030
GO:0034418 Urate biosynthetic process Increases phenotype PMID:30794797
GO:0034440 Lipid oxidation Increases phenotype PMID:10647909; PMID:30273961; PMID:30500344
GO:0042116 Macrophage activation Increases phenotype PMID:29352974
GO:0042310 Vasoconstriction Increases phenotype PMID:25169908
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:37263553
GO:0044237 Cellular metabolic process Decreases phenotype PMID:30445784; PMID:30578657; PMID:34774662
GO:0044319 Wound healing, spreading of cells Decreases phenotype PMID:30578657
GO:0045930 Negative regulation of mitotic cell cycle Increases phenotype PMID:29352974
GO:0046323 Glucose import Increases phenotype PMID:30445784
GO:0046326 Positive regulation of glucose import Decreases phenotype PMID:25719685
GO:0046415 Urate metabolic process Affects phenotype PMID:30794797
GO:0046449 Creatinine metabolic process Affects phenotype PMID:37057715
GO:0046618 Xenobiotic export from cell Decreases phenotype PMID:28458011
GO:0048873 Homeostasis of number of cells within a tissue Decreases phenotype PMID:35779630
GO:0050765 Negative regulation of phagocytosis Increases phenotype PMID:36114367
GO:0050996 Positive regulation of lipid catabolic process Increases phenotype PMID:37263553; PMID:38432408
GO:0051782 Negative regulation of cell division Increases phenotype PMID:35779630
GO:0060231 Mesenchymal to epithelial transition Increases phenotype PMID:24122885
GO:0061951 Establishment of protein localization to plasma membrane Increases phenotype PMID:30591588
GO:0070265 Necrotic cell death Increases phenotype PMID:34774662
GO:0071243 Cellular response to arsenic-containing substance Increases phenotype PMID:28458011
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:32220030; PMID:34774662
GO:0097272 Ammonium homeostasis Decreases phenotype PMID:30500344
GO:0140042 Lipid droplet formation Increases phenotype PMID:30445784; PMID:32220030
GO:1901216 Positive regulation of neuron death Increases phenotype PMID:30500344
GO:1901318 Negative regulation of flagellated sperm motility Increases phenotype PMID:30273961
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:30273961
GO:1903283 Negative regulation of glutathione peroxidase activity Increases phenotype PMID:30273961
GO:1903284 Positive regulation of glutathione peroxidase activity Decreases phenotype PMID:10647909
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:25169908

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.