Render Target: SSR
Render Timestamp: 2024-11-14T22:36:09.438Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-08-01 15:24:03.543
Product last modified at: 2024-08-26T12:00:17.421Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

AMPA Receptor 3 (GluA 3) Antibody #3437

Filter:
  • WB
  • IP

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 100
    SOURCE Rabbit
    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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    AMPA Receptor 3 (GluA 3) Antibody detects endogenous levels of total GluA 3 protein. The antibody is not predicted to detect other AMPA receptors subunits (e.g. GluA 1, GluA 2 or GluA 4) based on sequence homology of the antigen.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro590 of human GluA 3. Antibodies are purified by protein A and peptide affinity chromatography.

    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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