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- Table of Contents
Information about Type I Mucolipidosis: 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 Type I Mucolipidosis shares some biological mechanisms with ataxia, beta-galactosidase-deficiency, edema, epilepsies-myoclonic, epilepsy, galactosialidosis, gangliosidoses, gangliosidosis-gm1, gaucher-disease, inborn-errors-of-metabolism, lactose-intolerance, lysosomal-storage-diseases, mucolipidoses, mucopolysaccharidoses, myoclonic-epilepsies-progressive, myoclonus, neuraminidase-1-deficiency, storage-disease, type-ii-mucolipidosis.
Among the many pathways, these few ones have gauged particular interests from scientists studying Type I Mucolipidosis, and have been seen in publications frequently: Cell Differentiation, Cell Proliferation, Chromatin Remodeling, Elastic Fiber Assembly, Endocytosis, Excretion, Exocytosis, Fatty Acid Oxidation, Habituation, Immune Response, Intracellular Transport, Localization, Lysosomal Transport, Methylation, Pathogenesis, Receptor-mediated Endocytosis, Reflex, Secretion, Transport, Urea Cycle
Quite a number of genes have been found to play important roles in Type I Mucolipidosis, such as AGA, CSTB, CTLA4, CTSA, CUX1, EGFL7, ELN, GLB1, HLA-DQA1, LAMP1, MTCH1, NEU1, NEU2, NEU3, NOD2, PMEL, PSAP, QPCT, SH3D19. 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.