|Datasheet||Specific References||Reviews||Related Products||Protocols|
|Vector Type||Mammalian Expression Vector|
|Expression Method||Constiutive, Stable / Transient|
|Selection In Mammalian Cells||Hygromycin|
A polyhistidine-tag is an amino acid motif in proteins that consists of at least five histidine (His) residues, often at the N- or C-terminus of the protein.
Polyhistidine-tags are often used for affinity purification of polyhistidine-tagged recombinant proteins expressed in Escherichia coli and other prokaryotic expression systems.
|Human GLA ORF mammalian expression plasmid, C-GFPSpark tag||HG12078-ACG|
|Human GLA ORF mammalian expression plasmid, C-OFPSpark / RFP tag||HG12078-ACR|
|Human GLA ORF mammalian expression plasmid, C-Flag tag||HG12078-CF|
|Human GLA ORF mammalian expression plasmid, C-His tag||HG12078-CH|
|Human GLA ORF mammalian expression plasmid, C-Myc tag||HG12078-CM|
|Human GLA ORF mammalian expression plasmid, C-HA tag||HG12078-CY|
|Human GLA Gene cDNA clone plasmid||HG12078-G|
|Human GLA ORF mammalian expression plasmid, N-Flag tag||HG12078-NF|
|Human GLA ORF mammalian expression plasmid, N-His tag||HG12078-NH|
|Human GLA ORF mammalian expression plasmid, N-Myc tag||HG12078-NM|
|Human GLA ORF mammalian expression plasmid, N-HA tag||HG12078-NY|
|Human GLA natural ORF mammalian expression plasmid||HG12078-UT|
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Alpha-galactosidase A, also known as Alpha-D-galactoside galactohydrolase, Alpha-D-galactosidase A, Melibiase and GLA, is a member of the glycosyl hydrolase 27 family. GLA is used as a long-term enzyme replacement therapy in patients with a confirmed diagnosis of Fabry disease. Defects in GLA are the cause of Fabry disease (FD) which is a rare X-linked sphingolipidosis disease where glycolipid accumulates in many tissues. The disease consists of an inborn error of glycosphingolipid catabolism. FD patients show systemic accumulation of globotriaoslyceramide (Gb3) and related glycosphingolipids in the plasma and cellular lysosomes throughout the body. Clinical recognition in males results from characteristic skin lesions (angiokeratomas) over the lower trunk. Patients may show ocular deposits, febrile episodes, and burning pain in the extremities. Death results from renal failure, cardiac or cerebral complications of hypertension or other vascular disease. Deficiency of GLA leads to the accumulation of glycosphingolipids in the vasculature leading to multiorgan pathology. In addition to well-described microvascular disease, deficiency of GLA is also characterized by premature macrovascular events such as stroke and possibly myocardial infarction.