Ammonium chloride


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000045 Autophagosome assembly Increases phenotype PMID:24262987; PMID:31310755
GO:0001649 Osteoblast differentiation Increases phenotype PMID:23111315
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:23111315
GO:0005776 Autophagosome Increases phenotype PMID:31310755
GO:0006309 Apoptotic dna fragmentation Increases phenotype PMID:31310755
GO:0006497 Protein lipidation Affects phenotype PMID:24262987; PMID:31690173; PMID:34560126; PMID:37257343
GO:0006739 Nadp metabolic process Increases phenotype PMID:31974165
GO:0006749 Glutathione metabolic process Increases phenotype PMID:30508503
GO:0006914 Autophagy Increases phenotype PMID:24262987; PMID:29908302; PMID:37257343
GO:0006915 Apoptotic process Increases phenotype PMID:20594614
GO:0010508 Positive regulation of autophagy Increases phenotype PMID:25446377
GO:0010917 Negative regulation of mitochondrial membrane potential Increases phenotype PMID:31310755
GO:0015723 Bilirubin transport Increases phenotype PMID:30508503
GO:0016049 Cell growth Decreases phenotype PMID:27867098
GO:0019249 Lactate biosynthetic process Affects phenotype PMID:31974165
GO:0019395 Fatty acid oxidation Increases phenotype PMID:24262987
GO:0019627 Urea metabolic process Increases phenotype PMID:22524704; PMID:32017919
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:31310755
GO:0030336 Negative regulation of cell migration Increases phenotype PMID:28068557
GO:0034440 Lipid oxidation Increases phenotype PMID:30508503
GO:0036164 Cell-abiotic substrate adhesion Decreases phenotype PMID:31310755
GO:0042307 Positive regulation of protein import into nucleus Increases phenotype PMID:30508503
GO:0042554 Superoxide anion generation Increases phenotype PMID:31310755
GO:0042919 Benzoate transport Decreases phenotype PMID:8140053
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:30508503
GO:0044237 Cellular metabolic process Decreases phenotype PMID:31310755; PMID:37257343; PMID:38101597
GO:0044754 Autolysosome Increases phenotype PMID:31310755
GO:0045851 Ph reduction Decreases phenotype PMID:31310755
GO:0046718 Viral entry into host cell Decreases phenotype PMID:33676899
GO:0051092 Positive regulation of nf-kappab transcription factor activity Increases phenotype PMID:30508503
GO:0051156 Glucose 6-phosphate metabolic process Increases phenotype PMID:31974165
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:38101597
GO:0061024 Membrane organization Decreases phenotype PMID:31310755
GO:0061621 Canonical glycolysis Increases phenotype PMID:31974165
GO:0061951 Establishment of protein localization to plasma membrane Increases phenotype PMID:30591588
GO:0070782 Phosphatidylserine exposure on apoptotic cell surface Increases phenotype PMID:31310755
GO:0070994 Detection of oxidative stress Increases phenotype PMID:23343352
GO:0097153 Cysteine-type endopeptidase activity involved in apoptotic process Increases phenotype PMID:31310755
GO:0097272 Ammonium homeostasis Decreases phenotype PMID:30508503
GO:0140042 Lipid droplet formation Increases phenotype PMID:24262987; PMID:30138652
GO:1900745 Positive regulation of p38mapk cascade Increases phenotype PMID:30508503
GO:1901098 Positive regulation of autophagosome maturation Increases phenotype PMID:29908302
GO:1901670 Negative regulation of superoxide dismutase activity Increases phenotype PMID:30508503
GO:1903283 Negative regulation of glutathione peroxidase activity Increases phenotype PMID:30508503
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:27867098; PMID:31310755
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:30508503
GO:1990764 Myofibroblast contraction Increases phenotype PMID:38703806
GO:2000786 Positive regulation of autophagosome assembly Increases phenotype PMID:26031332; PMID:31927068
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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.