Pyridaben


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0002157 Positive regulation of thyroid hormone mediated signaling pathway Increases phenotype PMID:30818834
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:37357870
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:37357870
GO:0004069 L-aspartate:2-oxoglutarate aminotransferase activity Increases phenotype PMID:37357870
GO:0004602 Glutathione peroxidase activity Increases phenotype PMID:37357870
GO:0006096 Glycolytic process Increases phenotype PMID:32607615
GO:0006915 Apoptotic process Increases phenotype PMID:37357870
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:19591892
GO:0008283 Cell population proliferation Affects phenotype PMID:34642769; PMID:37357870
GO:0009060 Aerobic respiration Affects phenotype PMID:26141520
GO:0010917 Negative regulation of mitochondrial membrane potential Increases phenotype PMID:30818834
GO:0034440 Lipid oxidation Increases phenotype PMID:37357870
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:26141520
GO:0044237 Cellular metabolic process Decreases phenotype PMID:32607615; PMID:34642769
GO:0045333 Cellular respiration Decreases phenotype PMID:32607615; PMID:33512557
GO:0046034 Atp metabolic process Affects phenotype PMID:33512557; PMID:34642769
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:32607615; PMID:32607615; PMID:34642769
GO:0061726 Mitochondrion disassembly Increases phenotype PMID:26141520
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:26141520
GO:1905448 Positive regulation of mitochondrial atp synthesis coupled electron transport Decreases phenotype PMID:26141520
GO:1990787 Negative regulation of hh target transcription factor activity Increases phenotype PMID:30818834
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.