Doxycycline


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:9972138
GO:0006915 Apoptotic process Increases phenotype PMID:9972138
GO:0007283 Spermatogenesis Affects phenotype PMID:7861548
GO:0008219 Cell death Decreases phenotype PMID:2326552
GO:0008610 Lipid biosynthetic process Increases phenotype PMID:27089845
GO:0019227 Neuronal action potential propagation Increases phenotype PMID:36565944
GO:0031175 Neuron projection development Increases phenotype PMID:33798505; PMID:36565944
GO:0043970 Histone h3-k9 acetylation Affects phenotype PMID:36565944
GO:0044154 Histone h3-k14 acetylation Affects phenotype PMID:36565944
GO:0044237 Cellular metabolic process Decreases phenotype PMID:38115220
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:38115220
GO:0098532 Histone h3-k27 trimethylation Affects phenotype PMID:36565944
GO:1903608 Protein localization to cytoplasmic stress granule Increases phenotype PMID:24019256

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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.