protein

GLA/alpha-Galactosidase A Protein, Mouse (HEK293, His)

HY-P73077

5 μg;10 μg;50 μg

60;100;280 USD

GLA/alpha-Galactosidase A Protein, Mouse (HEK293, His)

proteins

HEK293

5 μg;10 μg;50 μg

60;100;280 USD

GLA/alpha-Galactosidase A Protein is responsible for the breakdown of alpha-galactoside in the lysosome. GLA/alpha-Galactosidase A Protein participates in the negative regulation of nitric oxide biosynthesis and nitric oxide synthase activity. A deficiency of GLA/alpha-Galactosidase A Protein causes Fabry disease. GLA/alpha-Galactosidase A Protein, Mouse (HEK293, His) is the recombinant mouse-derived GLA/alpha-Galactosidase A protein, expressed by HEK293 , with C-His labeled tag. The total length of GLA/alpha-Galactosidase A Protein, Mouse (HEK293, His) is 388 a.a., with molecular weight of 46-52 kDa.

Mouse

Alpha-galactosidase A is responsible for the breakdown of alpha-galactoside in lysosomes and is homologous to human galactosidase (GLA). GLA is involved in the negative regulation of nitric oxide biosynthesis and nitric oxide synthase activity. GLA acts upstream or internally in the catabolic process of glycosylceramide. Mice deficient in alpha-galactosidase A exhibit age-dependent and distinct sensory system deficits. This is a lysosome storage disorder characterized by the accumulation of alpha-galactosylated substrates in tissues. Alpha-galactosidase A is an active target of clinical research: there are currently two treatment options for Fabry disease, recombinant enzyme replacement therapy and drug companion therapy. Tlr-dependent alpha-Gal-A negative regulation is the mechanistic link between pathogen recognition and autolipid antigen induction in NKT cells [1] [2] [3] [4] .

Alpha-Galactosidase A; GALA; GLA; Melibiase

Greater than 95% as determined by reducing SDS-PAGE

Lyophilized from a 0.2 μm filtered solution of PBS, pH 7.4.

Room temperature in continental US; may vary elsewhere.