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PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a
  1. Products /
  2. Primary Antibodies /
  3. Silent Synapses Antibody Sampler Kit

Silent Synapses Antibody Sampler Kit #82760

    Product Information

    Kit Usage Information

    Protocols

    Product Description

    The Silent Synapses Antibody Sampler Kit provides an economical means of detecting the activation of AMPA-type glutamate receptors (AMPAR) using phospho-specific and control antibodies. AMPARs expression can be compared to other synaptic components including NMDA-type glutamate receptor subunit GluN1 and the synaptic scaffolding protein PSD95. The kit includes enough antibody to perform two western blot experiments with each primary antibody.

    Specificity / Sensitivity

    Each antibody in the Silent Synapses Antibody Sampler Kit detects its target protein at endogenous levels. The phospho-specific antibodies recognize
    human AMPA Receptor 1 (GluA1) only when phosphorylated at the indicated residues. While the literature refers to the GluA1 phospho-residues as Ser831 and Ser845, the corresponding residues for UniProt ID #P42261 are Ser849 and Ser863, respectively.

    Source / Purification

    Monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding Ala275 of human AMPA Receptor 1 (GluA1) protein, Ser52 of human AMPA Receptor 2 (GluA2) protein, Gln53 of human PSD95, and Pro660 of the human NMDA Receptor 1 (GluN1) protein. Activation-state specific monoclonal antibodies are produced by immunizing animals with synthetic phosphopeptides corresponding to residues surrounding Ser831 and Ser845 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 composed of four subunits (GluA1-4), 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 GluA2-containing AMPARs, AMPARs that lack GluA2 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 and surface expression of AMPARs representing key pathways to mediate synaptic plasticity (3). During development and mature states, some synapses exhibit “silent synapses” that lack functional AMPAR-mediated transmission. Synapses become “unsilenced” by post-translational modification of GluAs, particularly GluA1, which alters its kinetic properties and/or surface expression while other synaptic components, such as other glutamate receptors like NMDARs and postsynaptic scaffolding proteins like PSD95, remain unaltered. Conversely, reducing the AMPAR kinetic properties and surface expression can silence synapses. Key post-translational modifications implicated in regulating these processes include phosphorylation of GluA1 at Ser831 and Ser845 (4). Research studies have implicated activity-dependent changes in AMPARs in a variety of diseases, including Alzheimer’s, amyotrophic lateral sclerosis (ALS), stroke, and epilepsy (1).

    Database Links

    UniProt ID: P42261 , P78352 , Q05586 , P42262


    Entrez-Gene Id: 2890 , 1742 , 2902 , 2891


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