Render Target: STATIC
Render Timestamp: 2024-11-21T13:47:56.034Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-05-10 06:22:20.468
Product last modified at: 2024-11-18T13:15:16.256Z
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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.

EAAT1 (D44E2) XP® Rabbit mAb #5684

Filter:
  • IF

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 58
    Source/Isotype Rabbit IgG
    Application Key:
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Immunofluorescence (Frozen) 1:100
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:200

    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

    EAAT1 (D44E2) XP® Rabbit mAb recognizes endogenous levels of total EAAT1 protein.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues near the amino terminus of human EAAT1 protein.

    Background

    Glutamate is the major excitatory neurotransmitter in the mammalian central nervous system. During neurotransmission, glutamate is released from vesicles of the pre-synaptic cell, and glutamate receptors (e.g., NMDA Receptor, AMPA Receptor) bind glutamate for activation at the opposing post-synaptic cell. Excitatory amino acid transporters (EAATs) regulate and maintain extracellular glutamate concentrations below excitotoxic levels. In addition, glutamate transporters may limit the duration of synaptic excitation by an electrogenic process in which the transmitter is cotransported with three sodium ions and one proton, followed by countertransport of a potassium ion. Five EAATs (EAAT1-5) are characterized: EAAT2 (GLT-1) is primarily expressed in astrocytes but is also expressed in neurons of the retina and during fetal development (1). Homozygous EAAT2 knockout mice have spontaneous, lethal seizures and an increased predisposition to acute cortical injury (2). PKC phosphorylates Ser113 of EAAT2 and coincides with glutamate transport (3).

    EAAT2 accounts for up to 90% of the total glutamate transport in brain while EAAT1 contributes the remaining 5-10% (4). The contribution of EAAT1 in neurotransmission is unclear since EAAT2 is much more abundant. However, EAAT1 expression is upregulated by increasing concentrations of glutamate in the media of cultured primary astrocytes, potentially giving this glutamate transporter additional importance (5). EAAT1 has neuroprotective potential following ischemia since reactive astrocytes and activated microglia express EAAT1 but not EAAT2 (6).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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