Boron


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:30997025
GO:0006094 Gluconeogenesis Increases phenotype PMID:30997025
GO:0006695 Cholesterol biosynthetic process Increases phenotype PMID:30997025
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:30997025
GO:0006915 Apoptotic process Increases phenotype PMID:33137424
GO:0016042 Lipid catabolic process Increases phenotype PMID:30997025
GO:0019432 Triglyceride biosynthetic process Increases phenotype PMID:30997025
GO:0046449 Creatinine metabolic process Increases phenotype PMID:30997025; PMID:35020164
GO:0046466 Membrane lipid catabolic process Increases phenotype PMID:36419211
GO:0046651 Lymphocyte proliferation Affects phenotype PMID:33137424
GO:0048589 Developmental growth Affects phenotype PMID:32392305
GO:0071735 Igg immunoglobulin complex Affects phenotype PMID:33137424
GO:0085029 Extracellular matrix assembly Increases phenotype PMID:38500399

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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.