Product nameAnti-Glucokinase antibody - N-terminal
See all Glucokinase primary antibodies
DescriptionRabbit polyclonal to Glucokinase - N-terminal
Tested applicationsSuitable for: ELISA, ICC/IF, WB, IHC-Pmore details
Species reactivityReacts with: Mouse, Rat, Human, Pig, Common marmoset
- Human breast carcinoma and hepatocarcinoma tissues; HepG2 and mouse liver tissue cell lysates.
Storage instructionsShipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C long term.
Storage bufferPreservative: 0.09% Sodium azide
Concentration information loading...
PurityProtein G purified
Purification notesab37796 was eluted out with both high and low pH buffers and neutralised immediately after elution, followed by dialysis against PBS.
- Pathways and Processes
- Metabolic signaling pathways
- Energy transfer pathways
- Energy Metabolism
Our Abpromise guarantee covers the use of ab37796 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|ICC/IF||Use a concentration of 1 - 5 µg/ml.|
|WB||1/100 - 1/500. Detects a band of approximately 65 kDa (predicted molecular weight: 52 kDa).|
|IHC-P||1/50 - 1/100.|
FunctionCatalyzes 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.
Tissue specificityIsoform 1 is expressed in pancreas. Isoform 2 and isoform 3 is expressed in liver.
Involvement in diseaseDefects 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.
Sequence similaritiesBelongs to the hexokinase family.
- Information by UniProt
- ATP:D-hexose 6-phosphotransferase antibody
- FGQTL3 antibody
- GCK antibody
All lanes : Anti-Glucokinase antibody - N-terminal (ab37796)
Lane 1 : Hep G2 cell lysate
Lane 2 : Mouse liver lysate
Predicted band size: 52 kDa
Observed band size: 65 kDa why is the actual band size different from the predicted?
Additional bands at: 30 kDa, 37 kDa, 50 kDa. We are unsure as to the identity of these extra bands.
Formalin fixed, paraffin embedded human breast carcinoma tissue using ab37796, followed by AEC staining.
ICC/IF image of ab37796 stained HeLa cells. The cells were 4% PFA fixed (10 min) and then incubated in 1%BSA / 10% normal goat serum / 0.3M glycine in 0.1% PBS-Tween for 1h to permeabilise the cells and block non-specific protein-protein interactions. The cells were then incubated with the antibody (ab37796, 1µg/ml) overnight at +4°C. The secondary antibody (green) was Alexa Fluor® 488 goat anti-rabbit IgG (H+L) used at a 1/1000 dilution for 1h. Alexa Fluor® 594 WGA was used to label plasma membranes (red) at a 1/200 dilution for 1h. DAPI was used to stain the cell nuclei (blue) at a concentration of 1.43µM.
This product has been referenced in:
- Taneera J et al. GNAS gene is an important regulator of insulin secretory capacity in pancreatic ß-cells. Gene 715:144028 (2019). Read more (PubMed: 31374326) »
- Shin H et al. Blockade of cannabinoid 1 receptor improves glucose responsiveness in pancreatic beta cells. J Cell Mol Med 22:2337-2345 (2018). WB ; Mouse . Read more (PubMed: 29431265) »