AMPA Receptor 1 (GluA1) (D4N9V) Rabbit mAb #13185
- WB
- IP
- IF
Supporting Data
REACTIVITY | M R |
SENSITIVITY | Endogenous |
MW (kDa) | 100 |
Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
- IF-Immunofluorescence
Species Cross-Reactivity Key:
- M-Mouse
- R-Rat
Product Information
Product Usage Information
Application | Dilution |
---|---|
Western Blotting | 1:1000 |
Simple Western™ | 1:10 - 1:50 |
Immunoprecipitation | 1:50 |
Immunofluorescence (Frozen) | 1:100 - 1:400 |
Storage
For a carrier free (BSA and azide free) version of this product see product #39325.
Protocol
Specificity / Sensitivity
AMPA Receptor 1 (GluA1) (D4N9V) Rabbit mAb recognizes endogenous levels of total AMPA Receptor 1 (GluA1) protein.
Species Reactivity:
Mouse, Rat
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey, Bovine, Dog
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala275 of human AMPA Receptor 1 (GluA1) protein.
Background
AMPA- (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid), kainate-, 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 central nervous system. AMPARs are implicated in synapse formation, stabilization, and plasticity (1). In contrast to GluR 2-containing AMPARs, AMPARs that lack GluR 2 are permeable to calcium (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 1 is necessary for expression of long-term potentiation (LTP) in the hippocampus and formation of short-term memory (3). Hippocampal GluR 1 is also involved in morphine-induced adaptive synaptic mechanisms (4).
Limited Uses
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