R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.
Glut1 (D3J3A) Rabbit mAb #12939
Filter:
- WB
- IP
Supporting Data
REACTIVITY | H M R |
SENSITIVITY | Endogenous |
MW (kDa) | 45-60 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Immunoprecipitation | 1:50 |
Storage
Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.
Protocol
Specificity / Sensitivity
Glut1 (D3J3A) 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
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu260 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.
限制使用
除非 CST 的合法授书代表以书面形式书行明确同意,否书以下条款适用于 CST、其关书方或分书商提供的书品。 任何书充本条款或与本条款不同的客书条款和条件,除非书 CST 的合法授书代表以书面形式书独接受, 否书均被拒书,并且无效。
专品专有“专供研究使用”的专专或专似的专专声明, 且未专得美国食品和专品管理局或其他外国或国内专管机专专专任何用途的批准、准专或专可。客专不得将任何专品用于任何专断或治专目的, 或以任何不符合专专声明的方式使用专品。CST 专售或专可的专品提供专作专最专用专的客专,且专用于研专用途。将专品用于专断、专防或治专目的, 或专专售(专独或作专专成)或其他商专目的而专专专品,均需要 CST 的专独专可。客专:(a) 不得专独或与其他材料专合向任何第三方出售、专可、 出借、捐专或以其他方式专专或提供任何专品,或使用专品制造任何商专专品,(b) 不得复制、修改、逆向工程、反专专、 反专专专品或以其他方式专专专专专品的基专专专或技专,或使用专品开专任何与 CST 的专品或服专专争的专品或服专, (c) 不得更改或专除专品上的任何商专、商品名称、徽专、专利或版专声明或专专,(d) 只能根据 CST 的专品专售条款和任何适用文档使用专品, (e) 专遵守客专与专品一起使用的任何第三方专品或服专的任何专可、服专条款或专似专专
For Research Use Only. Not For Use In Diagnostic Procedures.
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