|Datasheet||Specific References||Reviews||Related Products||Protocols|
|A DNA sequence encoding the human BLK (NP_001706.2) (Met 1-Pro 505) was fused with the GST tag at the N-terminus.|
|Kinases are highly recommended to be shipped at frozen temperature with blue ice or dry ice.|
Shipment made at ambient temperature may seriously affect the activity of the ordered products.
|> 88 % as determined by SDS-PAGE|
|The specific activity was determined to be 17.4 nmol/min/mg using Poly(Glu,Tyr)4:1 peptide as substrate.|
|< 1.0 EU per μg of the protein as determined by the LAL method|
|Samples are stable for up to twelve months from date of receipt at -70℃|
|The recombinant human BLK/GST chimera consists of 730 amino acids and migrates as an approximatly 84 kDa band as predicted in SDS-PAGE under reducing conditions.|
|Supplied as sterile 20mM Tris, 500mM NaCl, 5mM GSH, pH 7.4|
1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
2. Please contact us for any concerns or special requirements.
|Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.|
|A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.|
Tyrosine-protein kinase Blk, also known as B lymphocyte kinase, p55-Blk and BLK, is a member of the protein kinase superfamily, Tyr protein kinase family and SRC subfamily. BLK / p55-Blk is expressed in lymphatic organs, pancreatic islets, Leydig cells, striate ducts of salivary glands and hair follicles. BLK / p55-Blk is a src-family protein tyrosine kinase specifically expressed in B-lineage cells of mice. The early onset of Blk expression during B-cell development in the bone marrow and the high expression levels of Blk in mature B cells suggest a possible important role of Blk in B-cell physiology. It is a modulator of beta-cells function, acting through the up-regulation of PDX1 and NKX6-1 and consequent stimulation of insulin secretion in response to glucose. Defects in BLK are a cause of maturity-onset diabetes of the young type 11 which is a form of diabetes that is characterized by an autosomal dominant mode of inheritance, onset in childhood or early adulthood (usually before 25 years of age), a primary defect in insulin secretion and frequent insulin-independence at the beginning of the disease.