The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
Biological Activity: 303 pmol/min/µg. One unit is defined as the amount of enzyme that will convert 1 pmol of NADP to NADPH at 30oC. Assay conditions: 25 mM HEPES, pH 7.5, 2 mM MgCl2, 1.0 mM DTT, 0.5 mM NADP, 2.0 mM ATP, 25 mM glucose, 100 µg/ml BSA, 20 units/ml glucose 6-phosphate dehydrogenase, and 10 nM human pancreatic glucokinase at 30°C for 30 min.
303 pmol/min/µg. One unit is defined as the amount of enzyme that will convert 1 pmol of NADP to NADPH at 30°C. Assay conditions: 25 mM HEPES, pH 7.5, 2 mM MgCl2, 1.0 mM DTT, 0.5 mM NADP, 2.0 mM ATP, 25 mM glucose, 100 µg/ml BSA, 20 units/ml glucose 6-phosphate dehydrogenase, and 10 nM human pancreatic glucokinase at 30°C for 30 min.
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Preparation and Storage
Stability and Storage
Shipped on dry ice. Upon delivery aliquot and store at -80ºC. Avoid freeze / thaw cycles.
This product is an active protein and may elicit a biological response in vivo, handle with caution.
Hexokinase D pancreatic isozyme
Hexokinase type IV
Catalyzes the initial step in utilization of glucose by the beta-cell and liver at physiological glucose concentration. Glucokinase has a high Km for glucose, and so it is effective only when glucose is abundant. The role of GCK is to provide G6P for the synthesis of glycogen. Pancreatic glucokinase plays an important role in modulating insulin secretion. Hepatic glucokinase helps to facilitate the uptake and conversion of glucose by acting as an insulin-sensitive determinant of hepatic glucose usage.
Isoform 1 is expressed in pancreas. Isoform 2 and isoform 3 is expressed in liver.
Involvement in disease
Defects in GCK are the cause of maturity-onset diabetes of the young type 2 (MODY2) [MIM:125851]; also shortened MODY-2. MODY 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. Defects in GCK are the cause of familial hyperinsulinemic hypoglycemia type 3 (HHF3) [MIM:602485]; also known as persistent hyperinsulinemic hypoglycemia of infancy (PHHI) or congenital hyperinsulinism. HHF is the most common cause of persistent hypoglycemia in infancy. Unless early and aggressive intervention is undertaken, brain damage from recurrent episodes of hypoglycemia may occur.