Recombinant Human BLK Protein (GST Tag)(Active)
SKU: PKSH030381-50
Recombinant Human BLK Protein (GST Tag)(Active)
SKU # | PKSH030381 |
Expression Host | Baculovirus-Insect Cells |
Description
Synonyms | B Lymphocyte Kinase, BLK, MODY11, Tyrosine-Protein Kinase Blk, p55-Blk |
Species | Human |
Expression Host | Baculovirus-Insect Cells |
Sequence | Met 1-Pro 505 |
Accession | NP_001706.2 |
Calculated Molecular Weight | 84 kDa |
Observed Molecular Weight | 84 kDa |
Tag | N-GST |
Bio-activity | The specific activity was determined to be 17.4 nmol/min/mg using Poly(Glu, Tyr)4:1 peptide as substrate. |
Properties
Purity | > 88 % as determined by reducing SDS-PAGE. |
Endotoxin | < 1.0 EU per μg of the protein as determined by the LAL method. |
Storage | Store at < -20°C, stable for 6 months. Please minimize freeze-thaw cycles. |
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. |
Formulation | Supplied as sterile solution of 20mM Tris, 500mM NaCl, 5mM GSH, pH 7.4 |
Reconstitution | Not Applicable |
Background
Tyrosine-protein kinase Blk, also known as B lymphocyte kinase, p55-Blk and BLK, is a member of theprotein 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.