Glut1 (E4S6I) Rabbit mAb (BSA and Azide Free) #84221
- WB
- 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
- IHC-Immunohistochemistry
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
- Mk-Monkey
Product Information
Product Usage Information
This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.
Formulation
Storage
Specificity / Sensitivity
Glut1 (E4S6I) Rabbit mAb (BSA and Azide Free) 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.
Limited Uses
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