AMPA Receptor 3 (GluA3) (D25G9) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0501

Target Information
UniProt ID	P42263

Product Details
Size	100 µL
Reactivity	Human, Mouse, Rat
Host	Rabbit
Source/Isotype	Rabbit IgG
Storage	Store at -20°C. Do not aliquot the antibody.
Purification	Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding His70 of human GluA3 protein.

Usage
Application	WB
Product Usage Information Dilution	Western Blotting (1:1000)
MW (Target)	100 kDa

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 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 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.

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 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 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.

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