Render Target: STATIC
Render Timestamp: 2024-12-20T12:23:37.501Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:53:34.980
Product last modified at: 2024-12-17T18:47:38.421Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
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).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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