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Disease Info Card
Hyperornithinemia
Information about Hyperornithinemia: 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 Hyperornithinemia
Most recent studies have shown that Hyperornithinemia shares some biological mechanisms with abnormal-degeneration, atrophy, blind-vision, cataract, chorioretinal-atrophy, disorder-of-eye, dystrophy, gyrate-atrophy, hyperammonemia, hyperornithinemia-hyperammonemia-homocitrullinuria-syndrome, inborn-errors-of-metabolism, metabolic-diseases, muscular-atrophy, myopia, phenylketonurias, retinal-degeneration, retinal-diseases, uveal-diseases.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperornithinemia, and have been seen in publications frequently: Antiport, Cell Death, Excretion, Fatty Acid Oxidation, Glycosylation, Localization, Mitochondrial Transport, Ornithine Transport, Pathogenesis, Reflex, Response To Vitamin, Response To Vitamin B6, Righting Reflex, Secretion, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Hyperornithinemia, such as AGA, AKR1C1, ALDH4A1, AMPD1, AMPD3, ATP8A2, DEFA1, ERG, GATM, GLS2, KCNH2, MTSS1, OAT, OTC, PRODH, SLC25A15. 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.