Phospho-AMPA Receptor 1 (GluA1) (Ser845) (D10G5) Rabbit Antibody

INQUIRY

CAT. NO.: AMA-0579

Target Information
UniProt ID	P42261

Product Details
Size	20 µL/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 phosphopeptide corresponding to residues surrounding Ser845 of human AMPA Receptor 1 (GluA1) protein.

Usage
Application	WB, IP
Product Usage Information Dilution	Western Blotting (1:1000); Immunoprecipitation (1:50)
MW (Target)	100 kDa

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 In contrast to GluR 2-containing AMPARs, AMPARs that lack GluR 2 are permeable to calcium 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 epilepsyThe activation of PKA regulates the activity of AMPA-type glutamate receptors by phosphorylation of the subunit GluR 1 at Ser845. Furthermore, Ser845 phosphorylation is increased by activation of D1-type dopamine receptors and by inhibition of protein phosphatase 1/protein phosphatase 2A Phosphorylation at either Ser831 or Ser845 potentiates AMPA receptor ion channel function: long-term potentiation (LTP) correlates with increased phosphorylation, while long-term depression (LTD) correlates with a dephosphorylation of GluR 1 Phosphomutant mice (Ser831Ala and Ser845Ala) show deficits in LTD and LTP. Either Ser831 or Ser845 alone may support LTP, while only Ser845 is critical for LTD. Furthermore, these mice have memory deficiencies in spatial learning tasks Assembly of the β2-adrenergic receptor, trimeric Gs protein, adenyl cyclase, PKA, GluR 1, stargazin, and PSD95 signaling complex for localized cAMP signaling is dependent on phosphorylation of GluR 1 at Ser845.

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 In contrast to GluR 2-containing AMPARs, AMPARs that lack GluR 2 are permeable to calcium 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 epilepsyThe activation of PKA regulates the activity of AMPA-type glutamate receptors by phosphorylation of the subunit GluR 1 at Ser845. Furthermore, Ser845 phosphorylation is increased by activation of D1-type dopamine receptors and by inhibition of protein phosphatase 1/protein phosphatase 2A Phosphorylation at either Ser831 or Ser845 potentiates AMPA receptor ion channel function: long-term potentiation (LTP) correlates with increased phosphorylation, while long-term depression (LTD) correlates with a dephosphorylation of GluR 1 Phosphomutant mice (Ser831Ala and Ser845Ala) show deficits in LTD and LTP. Either Ser831 or Ser845 alone may support LTP, while only Ser845 is critical for LTD. Furthermore, these mice have memory deficiencies in spatial learning tasks Assembly of the β2-adrenergic receptor, trimeric Gs protein, adenyl cyclase, PKA, GluR 1, stargazin, and PSD95 signaling complex for localized cAMP signaling is dependent on phosphorylation of GluR 1 at Ser845.

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