2,2',4,4',5-Pentabromodiphenyl ether


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001780 Neutrophil homeostasis Affects phenotype PMID:38648751
GO:0004096 Catalase activity Decreases phenotype PMID:20223270
GO:0004784 Superoxide dismutase activity Increases phenotype PMID:20223270
GO:0006171 Camp biosynthetic process Increases phenotype PMID:29790728
GO:0007611 Learning or memory Decreases phenotype PMID:17982161
GO:0007626 Locomotory behavior Affects phenotype PMID:21782714; PMID:21783602
GO:0008283 Cell population proliferation Decreases phenotype PMID:24451063
GO:0008344 Adult locomotory behavior Decreases phenotype PMID:17982161
GO:0010001 Glial cell differentiation Increases phenotype PMID:28851516
GO:0010468 Regulation of gene expression Affects phenotype PMID:38648751
GO:0010890 Positive regulation of sequestering of triglyceride Increases phenotype PMID:30903904
GO:0010942 Positive regulation of cell death Increases phenotype PMID:18550172; PMID:27015953; PMID:30202865
GO:0016477 Cell migration Decreases phenotype PMID:33969458
GO:0019058 Viral life cycle Affects phenotype PMID:23427858
GO:0030182 Neuron differentiation Decreases phenotype PMID:28851516
GO:0031987 Locomotion involved in locomotory behavior Affects phenotype PMID:26254212
GO:0032125 Micronucleus organization Increases phenotype PMID:39515574
GO:0034599 Cellular response to oxidative stress Increases phenotype PMID:20223270; PMID:20223270; PMID:24218147
GO:0034614 Cellular response to reactive oxygen species Increases phenotype PMID:24218147
GO:0036269 Swimming behavior Decreases phenotype PMID:17982161
GO:0042403 Thyroid hormone metabolic process Affects phenotype PMID:22759492
GO:0042445 Hormone metabolic process Affects phenotype PMID:23333513
GO:0042632 Cholesterol homeostasis Affects phenotype PMID:34425642
GO:0043491 Protein kinase b signaling Increases phenotype PMID:24218147
GO:0044319 Wound healing, spreading of cells Increases phenotype PMID:29790728
GO:0045600 Positive regulation of fat cell differentiation Increases phenotype PMID:30903904
GO:0045851 Ph reduction Increases phenotype PMID:31622892
GO:0045931 Positive regulation of mitotic cell cycle Increases phenotype PMID:30903904
GO:0048709 Oligodendrocyte differentiation Decreases phenotype PMID:33969458
GO:0048874 Host-mediated regulation of intestinal microbiota composition Affects phenotype PMID:38648751
GO:0051348 Negative regulation of transferase activity Affects phenotype PMID:29331935
GO:0051923 Sulfation Decreases phenotype PMID:29331935
GO:0070346 Positive regulation of fat cell proliferation Increases phenotype PMID:30903904
GO:0070633 Transepithelial transport Increases phenotype PMID:31622892
GO:0071897 Dna biosynthetic process Increases phenotype PMID:39668266
GO:1901671 Positive regulation of superoxide dismutase activity Increases phenotype PMID:20223270
GO:1902255 Positive regulation of intrinsic apoptotic signaling pathway by p53 class mediator Increases phenotype PMID:15475174
GO:1902552 Negative regulation of catalase activity Increases phenotype PMID:20223270
GO:1904358 Positive regulation of telomere maintenance via telomere lengthening Increases phenotype PMID:34193151
GO:2000448 Positive regulation of macrophage migration inhibitory factor signaling pathway Increases phenotype PMID:38648751
GO:2000609 Regulation of thyroid hormone generation Affects phenotype PMID:25965908; PMID:39626304
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.