Description
Recombinant Human BLK Protein (GST Tag)(Active) | PKSH030381 | Gentaur US, UK & Europe Disrtribition
Synonyms: Tyrosine-Protein Kinase Blk; B Lymphocyte Kinase; p55-Blk; BLK;MODY11
Active Protein: Active protein
Activity: A DNA sequence encoding the human BLK (NP_001706.2) (Met 1-Pro 505) was fused with the GST tag at the N-terminus.
Protein Construction: A DNA sequence encoding the human BLK (NP_001706.2) (Met 1-Pro 505) was fused with the GST tag at the N-terminus.
Fusion Tag: N-GST
Species: Human
Expressed Host: Baculovirus-Insect Cells
Shipping: This product is provided as liquid. It is shipped at frozen temperature with blue ice/gel packs. Upon receipt, store it immediately at<-20°C.
Purity: > 90 % as determined by reducing SDS-PAGE.
Endotoxin: < 1.0 EU per µg of the protein as determined by the LAL method.
Stability and Storage: Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles.
Molecular Mass: N/A
Formulation: Supplied as sterile 20mM Tris, 300mM NaCl, 0.5mM GSH, pH 7.5, 25% glycerol.
Reconstitution: Not Applicable
Background: 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.
Research Area: Cell biology
