Cell Signaling Technology

Product Pathways - Neuroscience

AMPA Receptor (GluR 4) (D19G9) Rabbit mAb #8010

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

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
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 4) (D19G9) Rabbit mAb recognizes endogenous levels of total GluR 4 protein. This antibody also detects background bands of unknown origin between 36 and 50 kDa.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg860 of human GluR 4 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from mouse brain and human cerebellum using AMPA Receptor (GluR 4) (D19G9) 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), which assemble as homo- or hetero-tetramers to mediate the majority of fast excitatory transmissions in the CNS. AMPARs are implicated in synapse formation, stabilization, and plasticity (1). AMPARs that lack GluR 2 are permeable to calcium, in contrast to GluR 2-containing AMPARs (2). Post-transcriptional modifications (alternative splicing, nuclear RNA editing) and post-translational modifications (glycosylation, phosphorylation) result in a very large number of permutations, fine-tuning the kinetic properties of AMPARs. Research studies have implicated activity changes in AMPARs in a variety of diseases including Alzheimer’s, amyotrophic lateral sclerosis (ALS), stroke, and epilepsy (1).

GluR 4 containing AMPARs are found in synapses and GluR 4 delivery to synapses and cell surface expression is mediated through phosphorylation of Ser842 by PKA or PKC (3).

  1. Palmer, C.L. et al. (2005) Pharmacol Rev 57, 253-77.
  2. Cull-Candy, S. et al. (2006) Curr Opin Neurobiol 16, 288-97.
  3. Gomes, A.R. et al. (2007) Traffic 8, 259-69.

Application References

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

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