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Disease Info Card
Hyperammonemia
Information about Hyperammonemia: characteristics, related genes and pathways, plus antibodies you can use for research. This page is being enriched constantly, if you see some information you would like this page to include please send your suggestions to us.
Overview of Hyperammonemia
Most recent studies have shown that Hyperammonemia shares some biological mechanisms with acidosis, brain-edema, citrullinemia, comatose, edema, encephalopathies, epilepsy, hepatic-encephalopathy, hyperammonaemic-encephalopathy, hypoglycemia, inborn-errors-of-metabolism, liver-cirrhosis, liver-diseases, liver-failure, liver-failure-acute, metabolic-diseases, ornithine-carbamoyltransferase-deficiency, urea-cycle-disorders-inborn.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperammonemia, and have been seen in publications frequently: Amino Acid Transport, Carnitine Transport, Coagulation, Conjugation, Excretion, Fatty Acid Oxidation, Gluconeogenesis, Glycolysis, Insulin Secretion, Intestinal Absorption, Localization, Locomotion, Ornithine Transport, Oxidative Phosphorylation, Pathogenesis, Proteolysis, Regeneration, Secretion, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Hyperammonemia, such as ABCC8, ALB, ASL, ASS1, CAT, CSF2, GLS, GLUD1, GLUL, H6PD, IL6, INS, LAMC2, NAGS, OTC, SEC14L2, SLC25A13, SLC25A15, UGDH. See what Boster has to offer for the research of these genes by clicking the gene name links below and view a more detailed info card/product listing for that gene.
In a later update, we will include information such as current drugs and therapy solutions as well as on-going and past clinical trials for this disease. Plesae stay updated.