Render Target: STATIC
Render Timestamp: 2024-11-21T12:52:15.136Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:55:40.704
Product last modified at: 2024-10-24T22:00:09.822Z
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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.

AMPA Receptor 3 (GluA3) (D25G9) Rabbit mAb #5117

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 100
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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

    AMPA Receptor 3 (GluA3) (D25G9) Rabbit mAb detects endogenous levels of total GluA3 protein. The antibody is not predicted to detect other AMPA receptor subunits (e.g. GluA1, GluA2 or GluA4) based on sequence homology of the antigen.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His70 of human GluA3 protein.

    Background

    AMPA- (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid), kainite- and NMDA- (N-methyl-D-aspartate) receptors are the three main families of ionotropic glutamate-gated ion channels. AMPA receptors (AMPARs) are comprised of four subunits (GluR 1-4) that assemble as homo- or hetero-tetramers and mediate the majority of fast excitatory transmissions in the CNS. AMPARs are implicated in synapse formation, stabilization and plasticity. Post-transcriptional modifications (alternative splicing and nuclear RNA editing) and post-translational modifications (glycosylation, phoshorylation) result in a very large number of permutations, fine-tuning the kinetic properties of AMPARs (1). GluR 3 knockout mice exhibited normal basal synaptic transmission and long-term depression (LTD) but enhanced long-term potentiation (LTP). In contrast, GluR 2/3 double knockout mice are impaired in basal synaptic transmission (2). Aberrant GluR 3 expression or activity is implicated in a number of diseases, including autoimmune epilepsy, X-linked mental retardation, Rett's syndrome, amyotrophic lateral sclerosis and Alzheimer disease (3).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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