|Calculated MW||H=52;M=52;Rat=52,50 KDa|
|Other Names||GCK; Glucokinase; Hexokinase type IV; Hexokinase-4; Hexokinase-D|
|Target/Specificity||This GCK antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 1-30 amino acids from the N-terminal region of human GCK.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||GCK Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||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.|
|Cellular Location||Cytoplasm. Nucleus. Note=Under low glucose concentrations, GCK associates with GKRP and the inactive complex is recruited to the hepatocyte nucleus|
|Tissue Location||Isoform 1 is expressed in pancreas. Isoform 2 and isoform 3 is expressed in liver|
Hexokinases phosphorylate glucose to produce glucose-6-phosphate, thus committing glucose to the glycolytic pathway. Alternative splicing of the gene for GCK results in three tissue-specific forms of glucokinase, one found in pancreatic islet beta cells and two found in liver. The protein localizes to the outer membrane of mitochondria. In contrast to other forms of hexokinase, this enzyme is not inhibited by its product glucose-6-phosphate but remains active while glucose is abundant. Mutations in the gene have been associated with non-insulin dependent diabetes mellitus (NIDDM), also called maturity onset diabetes of the young, type 2 (MODY2); mutations have also been associated with persistent hyperinsulinemic hypoglycemia of infancy (PHHI).
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Cao, H., et al., Hum. Mutat. 20(6):478-479 (2002).
Barrio, R., et al., J. Clin. Endocrinol. Metab. 87(6):2532-2539 (2002).