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Recombinant Human BLK Protein (GST Tag)(Active)– MSE Supplies LLC

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Recombinant Human BLK Protein (GST Tag)(Active)

SKU: PKSH030381-50

  • $ 64595



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.