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GLUT2 Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application 
| WB, ICC |
|---|---|
| Primary Accession | P11168 |
| Other Accession | NP_000331.1 |
| Host | Rabbit |
| Reactivity | Human |
| Clonality | Polyclonal |
| Description | Rabbit Anti-Human GLUT2 Polyclonal |
| Target/Specificity | Predicted molecular weight at ~57.5kDa. Observed molecular weight at 60-70kDa and 38-45kDa. |
| Other Names | Glucose Transporter 2 Antibody, Glucose Transporter GLUT2 Antibody, BLUT-2 Antibody, GTR_Human Antibody, SLC2a2 Antibody, Solute Carrier Family 2 (facilitated glucose transporter) member 2 Antibody |
| Immunogen | Synthetic peptide from the C-terminal of human GLUT2 |
| Purification | Peptide Affinity Purified |
| Storage | -20ºC |
| Storage Buffer | PBS, 50% glycerol, 0.09% sodium azide |
| Shipping Temperature | Blue Ice or 4ºC |
| Certificate of Analysis | A 1:1000 dilution of SPC-697 was sufficient for detection of GLUT2 on 293T Rapamycin-treated lysates using Goat anti-rabbit IgG:HRP as the secondary antibody. |
| Cellular Localization | Membrane |
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Provided below are standard protocols that you may find useful for product applications.
Background
Glucose transporter 2 (GLUT2) also known as solute carrier family 2 (facilitated glucose transporter), member 2 (SLC2A2) is a transmembrane carrier protein that enables protein facilitated glucose movement across cell membranes. It is the principal transporter for transfer of glucose between liver and blood, and has a role in renal glucose reabsorption (1). Mutations in SLC2A2 lead to Fanconi-Bickel syndrome (FBS), which results in hepatorenal glycogen accumulation, proximal renal tubular dysfunction, and impaired utilization of glucose and galactose. Recent studies have shown that mutations in SLC2A2 can cause neonatal diabetes, and therefore may contribute to human insulin secretion (2). Novel SLC2A2 mutations have also been discovered and are being investigated to determine their roles in FBS as well (3).
References
1. Kellett G.L., Brot-Laroche E. (2005) Diabetes. 54(10): 3056-3062.
2. Sansbury F.H., et al. (2012) Diabetologia. 55(9): 2381-2385.
3. Su Z., et al. (2011) J Perdiatr Endocrinol Metab. 24(9-10): 749-753.
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