Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome

Overview of Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome

Most recent studies have shown that Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome shares some biological mechanisms with ataxia, atrophy, brain-injuries, cerebellar-ataxia, citrullinemia, comatose, gait-abnormality, gyrate-atrophy, hyperammonemia, hyperornithinemia, inborn-errors-of-metabolism, lysinuric-protein-intolerance, metabolic-diseases, mitochondrial-diseases, paraparesis, paraparesis-spastic.

Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome, and have been seen in publications frequently: Excretion, Lipid Oxidation, Localization, Muscle Atrophy, Ornithine Transport, Oxidative Phosphorylation, Pathogenesis, Reflex, Reverse Transcription, Righting Reflex, Secretion, Transport, Urea Cycle

Quite a number of genes have been found to play important roles in Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome, such as ADI1, ADSL, ASL, ASS1, ATP8A2, CAT, ITGA2B, ITGB3, LAMC2, OAT, ORC1, ORC2, OTC, POMT1, SLC25A15, SLC25A2, SLC25A29. 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.

Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome Related Genes

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Pathways Related to Hyperornithinemia-hyperammonemia-homocitrullinuria Syndrome

This information is being compiled and will come in a future update

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