Product Pathways - Neuroscience
AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb #13185
|13185S||100 µl (10 western blots)||---||In Stock||---|
|13185||carrier free and custom formulation / quantity||email request|
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|W||1:1000||Human, Mouse, Rat||Endogenous||100||Rabbit IgG|
Species cross-reactivity is determined by western blot.
Applications Key: W=Western Blotting, IP=Immunoprecipitation, IF-F=Immunofluorescence (Frozen)
Species predicted to react based on 100% sequence homology: Monkey, Bovine, Dog.
Specificity / Sensitivity
AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb recognizes endogenous levels of total AMPA Receptor (GluR 1) protein.
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala275 of human AMPA Receptor (GluR 1) protein.
Western blot analysis of extracts from mouse brain, rat brain, and rat prefrontal cortex tissues using AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb.
Immunoprecipitation of AMPA Receptor (GluR 1) from mouse brain extracts, using Rabbit (DA1E) mAb IgG XP® Isotype Control #3900 (lane 2) or AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb (lane 3). Lane 1 is 10% input. Western blot analysis was performed using AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb.
Confocal immunofluorescent analysis of mouse hippocampus using AMPA Receptor (GluR 1) (D4N9V) Rabbit mAb (green). Blue pseudocolor = DRAQ5® #4084 (fluorescent DNA dye).
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).
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