Dichloromethane


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0002693 Positive regulation of cellular extravasation Increases phenotype PMID:29335169
GO:0004364 Glutathione transferase activity Increases phenotype PMID:9794803
GO:0006974 Cellular response to dna damage stimulus Increases phenotype PMID:34280354
GO:0007204 Positive regulation of cytosolic calcium ion concentration Increases phenotype PMID:23559643; PMID:30503853
GO:0008284 Positive regulation of cell population proliferation Decreases phenotype PMID:23559643
GO:0016477 Cell migration Increases phenotype PMID:34280354
GO:0032922 Circadian regulation of gene expression Affects phenotype PMID:28392392
GO:0034440 Lipid oxidation Affects phenotype PMID:29335169
GO:0034465 Response to carbon monoxide Increases phenotype PMID:28392392
GO:0036164 Cell-abiotic substrate adhesion Decreases phenotype PMID:34280354
GO:0046034 Atp metabolic process Affects phenotype PMID:30240022
GO:0050729 Positive regulation of inflammatory response Increases phenotype PMID:29335169
GO:0060326 Cell chemotaxis Increases phenotype PMID:34280354
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:23559643
GO:2000391 Positive regulation of neutrophil extravasation Increases phenotype PMID:29335169
DISCLAIMER

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.