Thymol


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000737 Dna catabolic process, endonucleolytic Increases phenotype PMID:35521929
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:34665902
GO:0003954 Nadh dehydrogenase activity Decreases phenotype PMID:26721194
GO:0004111 Creatine kinase activity Affects phenotype PMID:26721194; PMID:30243740
GO:0004364 Glutathione transferase activity Decreases phenotype PMID:26680107
GO:0004448 Isocitrate dehydrogenase [nad(p)+] activity Decreases phenotype PMID:26721194
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:26721194
GO:0004602 Glutathione peroxidase activity Decreases phenotype PMID:26680107; PMID:26721194; PMID:26996544
GO:0004784 Superoxide dismutase activity Affects phenotype PMID:26680107; PMID:26721194; PMID:34171690; PMID:35521929
GO:0006749 Glutathione metabolic process Affects phenotype PMID:26801986; PMID:34171690; PMID:35521929
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:26680107; PMID:26721194; PMID:26996544
GO:0006754 Atp biosynthetic process Decreases phenotype PMID:26721194
GO:0007254 Jnk cascade Increases phenotype PMID:30048646
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:26801986; PMID:9164984
GO:0010189 Vitamin e biosynthetic process Decreases phenotype PMID:26680107; PMID:26996544
GO:0016042 Lipid catabolic process Increases phenotype PMID:26680107; PMID:26721194; PMID:26996544; PMID:30243740; PMID:35521929
GO:0016615 Malate dehydrogenase activity Decreases phenotype PMID:26721194
GO:0019432 Triglyceride biosynthetic process Increases phenotype PMID:26680107; PMID:26721194
GO:0019853 L-ascorbic acid biosynthetic process Decreases phenotype PMID:26680107; PMID:26996544
GO:0032148 Activation of protein kinase b activity Increases phenotype PMID:30048646
GO:0034440 Lipid oxidation Increases phenotype PMID:106178
GO:0042756 Drinking behavior Affects phenotype PMID:34665902
GO:0044237 Cellular metabolic process Decreases phenotype PMID:35521929
GO:0045429 Positive regulation of nitric oxide biosynthetic process Increases phenotype PMID:36535314
GO:0045672 Positive regulation of osteoclast differentiation Increases phenotype PMID:30048646
GO:0045780 Positive regulation of bone resorption Increases phenotype PMID:30048646
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:26801986
GO:0055088 Lipid homeostasis Affects phenotype PMID:36535314
GO:0061370 Testosterone biosynthetic process Affects phenotype PMID:34171690
GO:0061726 Mitochondrion disassembly Increases phenotype PMID:26721194
GO:0070328 Triglyceride homeostasis Affects phenotype PMID:36535314
GO:0070994 Detection of oxidative stress Increases phenotype PMID:34171690; PMID:34665902
GO:0071848 Positive regulation of erk1 and erk2 cascade via tnfsf11-mediated signaling Increases phenotype PMID:30048646
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:35521929
GO:0097722 Sperm motility Decreases phenotype PMID:34171690
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:26801986
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:30243740
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:36535314
GO:1905665 Positive regulation of calcium ion import across plasma membrane Increases phenotype PMID:28945920
GO:2000786 Positive regulation of autophagosome assembly Increases phenotype PMID:36535314
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.