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- Table of Contents
Information about Succinate-semialdehyde Dehydrogenase Deficiency: 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 Succinate-semialdehyde Dehydrogenase Deficiency shares some biological mechanisms with absence-epilepsy, ataxia, atrophy, brain-diseases-metabolic, brain-diseases-metabolic-inborn, convulsions, developmental-delay-(disorder), developmental-disabilities, epilepsy, globus-hystericus, inborn-errors-of-metabolism, metabolic-diseases, muscle-hypotonia, nervous-system-disorder, nervousness, sleep-disorders, status-epilepticus.
Among the many pathways, these few ones have gauged particular interests from scientists studying Succinate-semialdehyde Dehydrogenase Deficiency, and have been seen in publications frequently: Central Nervous System Development, Creatine Transport, Dna Amplification, Excretion, Glycosylation, Light Absorption, Localization, Myelination, Nervous System Development, Pathogenesis, Pyruvate Oxidation, Response To Reactive Oxygen Species, Reverse Transcription, Sensory Processing, System Development, Translation, Transport, Tricarboxylic Acid Cycle, Urea Cycle
Quite a number of genes have been found to play important roles in Succinate-semialdehyde Dehydrogenase Deficiency, such as ABAT, ACAT1, ALDH5A1, CALR, CAT, CDKN2A, CRAT, CSF2, ECHDC1, GAD1, GLUL, GLYAT, LAMC2, S100A9, SOD1, TRIM21, USB1. 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.