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Disease Info Card
Hyperlysinemias
Information about Hyperlysinemias: 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 Hyperlysinemias
Most recent studies have shown that Hyperlysinemias shares some biological mechanisms with acidemia, acidosis, citrullinemia, comatose, convulsions, hyperammonemia, hyperargininemia, inborn-errors-of-metabolism, metabolic-diseases, muscle-hypotonia, ornithine-carbamoyltransferase-deficiency, persistent-hyperlysinemia, propionic-acidemia, pyruvate-carboxylase-deficiency-disease, renal-aminoacidurias.
Among the many pathways, these few ones have gauged particular interests from scientists studying Hyperlysinemias, and have been seen in publications frequently: Excretion, Fatty Acid Beta-oxidation, Fatty Acid Oxidation, Lysine Transport, Mating, Pathogenesis, Rna Interference, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Hyperlysinemias, such as AASS, ALDH7A1, AMY2A, ASS1, CELA3B, CHKA, CSF2, DLD, ECHDC1, ENOPH1, EPB42, L2HGDH, LAMC2, OTC, PC, PRH1, SLC7A7. 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.
Pathways Related to Hyperlysinemias
This information is being compiled and will come in a future update
| Excretion | Fatty Acid Beta oxidation | Fatty Acid Oxidation |
| Lysine Transport | Mating | Pathogenesis |
| Rna Interference | Transport | Urea Cycle |