Acetochlor


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:19591892
GO:0010424 Dna methylation on cytosine within a cg sequence Affects phenotype PMID:34516295
GO:0035932 Aldosterone secretion Affects phenotype PMID:31524045
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:25291404
GO:0045600 Positive regulation of fat cell differentiation Increases phenotype PMID:39240656
GO:0051091 Positive regulation of dna-binding transcription factor activity Increases phenotype PMID:28973306
GO:0070374 Positive regulation of erk1 and erk2 cascade Increases phenotype PMID:25291404
GO:0090200 Positive regulation of release of cytochrome c from mitochondria Increases phenotype PMID:25291404
GO:0140042 Lipid droplet formation Increases phenotype PMID:39240656
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:25291404
GO:2000611 Positive regulation of thyroid hormone generation Increases phenotype PMID:31362416
GO:2001244 Positive regulation of intrinsic apoptotic signaling pathway Increases phenotype PMID:25291404
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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.