Carbon


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0001892 Embryonic placenta development Decreases phenotype PMID:33603097
GO:0006954 Inflammatory response Increases phenotype PMID:23717615
GO:0007204 Positive regulation of cytosolic calcium ion concentration Increases phenotype PMID:27939335
GO:0007613 Memory Decreases phenotype PMID:27128166
GO:0008016 Regulation of heart contraction Affects phenotype PMID:26276052
GO:0008217 Regulation of blood pressure Affects phenotype PMID:26276052
GO:0010467 Gene expression Affects phenotype PMID:25564368
GO:0010468 Regulation of gene expression Affects phenotype PMID:27809917
GO:0010508 Positive regulation of autophagy Increases phenotype PMID:25979628
GO:0018159 Peptidyl-methionine oxidation Increases phenotype PMID:25979628
GO:0030216 Keratinocyte differentiation Affects phenotype PMID:31791492
GO:0032731 Positive regulation of interleukin-1 beta production Increases phenotype PMID:26276052
GO:0044319 Wound healing, spreading of cells Increases phenotype PMID:26880698
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:34417545
GO:0060047 Heart contraction Affects phenotype PMID:20595912
GO:0060326 Cell chemotaxis Increases phenotype PMID:26880698
GO:0060964 Regulation of mirna-mediated gene silencing Affects phenotype PMID:26068961
GO:0070374 Positive regulation of erk1 and erk2 cascade Increases phenotype PMID:25979628

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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.