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The pGEM-T is 3kb in length, and contains the amplicin resistance gene, conferring selection of the plasmid in E. coli, and the ori site which is the bacterial origin of replication. The plasmid has multiple cloning sites as shown below. The coding sequence was inserted by TA cloning. Many E. coli strains are suitable for the propagation of this vector including JM109, DH5α and TOP10.
The coding sequence can be easily obtained by digesting the vector with proper restriction enzyme(s). The coding sequence can also be amplified by PCR with M13 primers, or primer pair SP6 and T7.
|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 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.