2,3',4,4',5-Pentachlorobiphenyl


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000045 Autophagosome assembly Increases phenotype PMID:31020377
GO:0001825 Blastocyst formation Decreases phenotype PMID:27417426
GO:0002440 Production of molecular mediator of immune response Increases phenotype PMID:18995849
GO:0002523 Leukocyte migration involved in inflammatory response Increases phenotype PMID:36450500
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:31251971
GO:0006590 Thyroid hormone generation Affects phenotype PMID:36450500
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:31251971
GO:0006914 Autophagy Increases phenotype PMID:31020377; PMID:32895711
GO:0007005 Mitochondrion organization Decreases phenotype PMID:36450500
GO:0007058 Spindle assembly involved in female meiosis ii Decreases phenotype PMID:31388691
GO:0007612 Learning Affects phenotype PMID:32521479
GO:0008283 Cell population proliferation Increases phenotype PMID:31251971
GO:0009566 Fertilization Decreases phenotype PMID:31388691
GO:0010942 Positive regulation of cell death Increases phenotype PMID:27417426
GO:0016049 Cell growth Decreases phenotype PMID:29704545
GO:0019659 Glucose catabolic process to lactate Increases phenotype PMID:31251971
GO:0030500 Regulation of bone mineralization Affects phenotype PMID:23816203
GO:0032204 Regulation of telomere maintenance Affects phenotype PMID:32300848
GO:0032237 Activation of store-operated calcium channel activity Increases phenotype PMID:32895711
GO:0032776 Dna methylation on cytosine Affects phenotype PMID:31388691
GO:0033327 Leydig cell differentiation Decreases phenotype PMID:27417426
GO:0040038 Polar body extrusion after meiotic divisions Decreases phenotype PMID:31388691
GO:0042403 Thyroid hormone metabolic process Affects phenotype PMID:19750101
GO:0043433 Negative regulation of dna-binding transcription factor activity Increases phenotype PMID:26022396
GO:0044027 Hypermethylation of cpg island Affects phenotype PMID:25585924
GO:0044237 Cellular metabolic process Increases phenotype PMID:31251971
GO:0045821 Positive regulation of glycolytic process Increases phenotype PMID:30821169
GO:0046330 Positive regulation of jnk cascade Increases phenotype PMID:26519956
GO:0050847 Progesterone receptor signaling pathway Decreases phenotype PMID:26022396
GO:0050890 Cognition Decreases phenotype PMID:18288320; PMID:20731829
GO:0051091 Positive regulation of dna-binding transcription factor activity Increases phenotype PMID:26022396
GO:0061370 Testosterone biosynthetic process Decreases phenotype PMID:27417426
GO:0070192 Chromosome organization involved in meiotic cell cycle Decreases phenotype PMID:31388691
GO:0070327 Thyroid hormone transport Decreases phenotype PMID:25644787
GO:0071407 Cellular response to organic cyclic compound Affects phenotype PMID:26022396; PMID:32199159
GO:0072593 Reactive oxygen species metabolic process Affects phenotype PMID:36450500
GO:0090116 C-5 methylation of cytosine Decreases phenotype PMID:31388691
GO:1900017 Positive regulation of cytokine production involved in inflammatory response Increases phenotype PMID:26519956
GO:1901522 Positive regulation of transcription from rna polymerase ii promoter involved in cellular response to chemical stimulus Increases phenotype PMID:26022396
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:30821169; PMID:31251971
GO:1904613 Cellular response to 2,3,7,8-tetrachlorodibenzodioxine Increases phenotype PMID:26022396
GO:2000020 Positive regulation of male gonad development Decreases phenotype PMID:27417426
GO:2000612 Regulation of thyroid-stimulating hormone secretion Affects phenotype PMID:19750101
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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.