Glut1 (E4S6I) Rabbit mAb #73015
- WB
- IP
- IHC
- IF
- F
Supporting Data
| REACTIVITY | H M R Mk |
| SENSITIVITY | Endogenous |
| MW (kDa) | 45-60 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:50 |
| Immunohistochemistry (Paraffin) | 1:250 - 1:1000 |
| Immunofluorescence (Frozen) | 1:50 - 1:200 |
| Immunofluorescence (Immunocytochemistry) | 1:50 - 1:200 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 - 1:200 |
Storage
For a carrier free (BSA and azide free) version of this product see product #84221.
Protocol
Specificity / Sensitivity
Glut1 (E4S6I) Rabbit mAb recognizes endogenous levels of total Glut1 protein. This antibody does not cross-react with Glut2, Glut3, or Glut4.
Species Reactivity:
Human, Mouse, Rat, Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the carboxy terminus of human Glut1 protein.
Background
Glucose transporter 1 (Glut1, SLC2A1) is a widely expressed transport protein that displays a broad range of substrate specificity in transporting a number of different aldose sugars as well as an oxidized form of vitamin C into cells (1,2). Glut1 is responsible for the basal-level uptake of glucose from the blood through facilitated diffusion (2). Research studies show that Glut1 and the transcription factor HIF-1α mediate the regulation of glycolysis by O-GlcNAcylation in cancer cells (3). Additional studies demonstrate that Glut1 is required for CD4 T cell activation and is critical for the expansion and survival of T effector (Teff) cells (4). Mutations in the corresponding SLC2A1 gene cause GLUT1 deficiency syndromes (GLUT1DS1, GLUT1DS2), a pair of neurologic disorders characterized by delayed development, seizures, spasticity, paroxysmal exercise-induced dyskinesia, and acquired microcephaly (5,6). Two other neurologic disorders - dystonia-9 (DYT9) and susceptibility to idiopathic generalized epilepsy 12 (EIG12) - are also caused by mutations in the SLC2A1 gene (7,8).
- Ferrer, C.M. et al. (2014) Mol Cell 54, 820-31.
- Deng, D. et al. (2014) Nature 510, 121-5.
- Agus, D.B. et al. (1997) J Clin Invest 100, 2842-8.
- Macintyre, A.N. et al. (2014) Cell Metab 20, 61-72.
- Wang, D. et al. (2005) Ann Neurol 57, 111-8.
- Schneider, S.A. et al. (2009) Mov Disord 24, 1684-8.
- Weber, Y.G. et al. (2011) Neurology 77, 959-64.
- Suls, A. et al. (2009) Ann Neurol 66, 415-9.
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