Gingerol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0003993 Acid phosphatase activity Decreases phenotype PMID:28421826
GO:0004035 Alkaline phosphatase activity Decreases phenotype PMID:28421826
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:28373059; PMID:31004597
GO:0004602 Glutathione peroxidase activity Affects phenotype PMID:28373059; PMID:28421826; PMID:33347680
GO:0004784 Superoxide dismutase activity Affects phenotype PMID:28373059; PMID:28421826; PMID:28988496; PMID:31004597; PMID:33347680
GO:0006606 Protein import into nucleus Affects phenotype PMID:33347680
GO:0006749 Glutathione metabolic process Increases phenotype PMID:28421826; PMID:28904557; PMID:28988496; PMID:33347680
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:28373059; PMID:31004597
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:28373059; PMID:31004597
GO:0006915 Apoptotic process Increases phenotype PMID:25034532; PMID:27451028; PMID:37121058
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:28988496
GO:0007283 Spermatogenesis Decreases phenotype PMID:28421826
GO:0008283 Cell population proliferation Decreases phenotype PMID:25034532; PMID:27451028
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:28249781
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:29555536
GO:0010884 Positive regulation of lipid storage Decreases phenotype PMID:26498061
GO:0014068 Positive regulation of phosphatidylinositol 3-kinase signaling Decreases phenotype PMID:28249781
GO:0016042 Lipid catabolic process Increases phenotype PMID:28373059; PMID:28421826; PMID:28988496; PMID:33347680
GO:0016477 Cell migration Affects phenotype PMID:32926756
GO:0019852 L-ascorbic acid metabolic process Affects phenotype PMID:33347680
GO:0030027 Lamellipodium Decreases phenotype PMID:32926756
GO:0032148 Activation of protein kinase b activity Decreases phenotype PMID:28249781
GO:0034440 Lipid oxidation Increases phenotype PMID:28904557; PMID:31004597
GO:0042360 Vitamin e metabolic process Affects phenotype PMID:33347680
GO:0042743 Hydrogen peroxide metabolic process Affects phenotype PMID:28421826
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:28249781
GO:0044237 Cellular metabolic process Decreases phenotype PMID:36341865; PMID:37121058
GO:0044319 Wound healing, spreading of cells Decreases phenotype PMID:32926756
GO:0045600 Positive regulation of fat cell differentiation Decreases phenotype PMID:26498061
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:28421826
GO:0050665 Hydrogen peroxide biosynthetic process Increases phenotype PMID:28373059
GO:0051726 Regulation of cell cycle Increases phenotype PMID:28249781
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:27451028; PMID:28988496
GO:0060740 Prostate gland epithelium morphogenesis Decreases phenotype PMID:28904557
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:28421826
GO:0071902 Positive regulation of protein serine/threonine kinase activity Increases phenotype PMID:28249781
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:25034532; PMID:28988496
GO:0090200 Positive regulation of release of cytochrome c from mitochondria Increases phenotype PMID:28249781
GO:0090263 Positive regulation of canonical wnt signaling pathway Increases phenotype PMID:26498061
GO:0097722 Sperm motility Decreases phenotype PMID:28421826
GO:1900744 Regulation of p38mapk cascade Affects phenotype PMID:28249781
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:27451028

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.