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- Table of Contents
Information about Sulfocysteinuria: 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.
Most recent studies have shown that Sulfocysteinuria shares some biological mechanisms with atrophy, brain-diseases-metabolic-inborn, cerebral-atrophy, combined-molybdoflavoprotein-enzyme-deficiency, congenital-ectopia, convulsion-neonatal, dislocations, ectopia-lentis, encephalopathies, hereditary-xanthinuria, hypoxia, inborn-errors-of-metabolism, lens-dislocation, lens-subluxation, metabolic-diseases, microcephaly.
Among the many pathways, these few ones have gauged particular interests from scientists studying Sulfocysteinuria, and have been seen in publications frequently: Electron Transport, Electron Transport Chain, Excretion, Fatty Acid Beta-oxidation, Fatty Acid Oxidation, Glomerular Filtration, Glycosylation, Hypersensitivity, Mating, Oxygen Transport, Platelet Aggregation, Translation, Transport, Transsulfuration, Tricarboxylic Acid Cycle, Urea Cycle
Quite a number of genes have been found to play important roles in Sulfocysteinuria, such as AOX1, ATRX, DHDDS, DHPS, GLUD1, GPHN, MOCS1, MOCS2, MOCS3, PRM1, PRPH2, SDS, SLC25A15, SOD1, SUOX, XDH. 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.