Dibutyldichlorotin


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:11097871
GO:0006754 Atp biosynthetic process Affects phenotype PMID:35435491
GO:0006915 Apoptotic process Increases phenotype PMID:11097871
GO:0006979 Response to oxidative stress Increases phenotype PMID:11097871
GO:0007224 Smoothened signaling pathway Decreases phenotype PMID:31652400
GO:0010508 Positive regulation of autophagy Increases phenotype PMID:30611790; PMID:37169277
GO:0019722 Calcium-mediated signaling Affects phenotype PMID:11097871
GO:0032148 Activation of protein kinase b activity Decreases phenotype PMID:30611790
GO:0032967 Positive regulation of collagen biosynthetic process Increases phenotype PMID:30611790
GO:0036394 Amylase secretion Increases phenotype PMID:37169277
GO:0044237 Cellular metabolic process Decreases phenotype PMID:31652400
GO:0044255 Cellular lipid metabolic process Affects phenotype PMID:34323617
GO:0045444 Fat cell differentiation Increases phenotype PMID:37142754
GO:0048384 Retinoic acid receptor signaling pathway Decreases phenotype PMID:31652400
GO:0050867 Positive regulation of cell activation Increases phenotype PMID:30611790
GO:0140042 Lipid droplet formation Increases phenotype PMID:37142754
GO:1901203 Positive regulation of extracellular matrix assembly Increases phenotype PMID:30611790
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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.