Cell Signaling Technology

Product Pathways - Neuroscience

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

Applications Reactivity Sensitivity MW (kDa) Isotype
W H M R Endogenous 100 Rabbit IgG

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

AMPA Receptor (GluR 3) (D25G9) Rabbit mAb detects endogenous levels of total GluR 3 protein. The antibody is not predicted to detect other AMPA receptor subunits (e.g. GluR 1, GluR 2 or GluR 4) based on sequence homology of the antigen.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His70 of human GluR 3 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse and rat brains using AMPA Receptor (GluR 3) (D25G9) Rabbit mAb.

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).

  1. Palmer, C.L. et al. (2005) Pharmacol Rev 57, 253-77.
  2. Meng, Y. et al. (2003) Neuron 39, 163-76.
  3. Rembach, A. et al. (2004) J Neurosci Res 77, 573-82.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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