Render Target: STATIC
Render Timestamp: 2024-11-21T13:18:12.955Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-05-10 22:31:07.471
Product last modified at: 2024-10-04T11:30:15.439Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

Glut1 (IHC404) Mouse mAb #71831

Filter:
  • IHC

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Mouse IgG2a
    Application Key:
    • IHC-Immunohistochemistry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Immunohistochemistry (Paraffin) 1:1600 - 1:3200

    Storage

    Supplied in a Tris-based buffer with 1% BSA and less than 0.1% sodium azide. Stable for 24 months when stored at 4°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Glut1 (IHC404) Mouse mAb recognizes endogenous levels of total Glut1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to the C terminal of 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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