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Merck
CN

AB2212

Anti-phospho GluR4 (S862) Antibody

serum, Chemicon®

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
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biological source

rabbit

antibody form

serum

antibody product type

primary antibodies

clone

polyclonal

species reactivity

rat

manufacturer/tradename

Chemicon®

technique(s)

western blot: suitable

UniProt accession no.

shipped in

wet ice

target post-translational modification

phosphorylation (pSer862)

Gene Information

human ... GRIA4(2893)

General description

Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes composed of multiple subunits, arranged to form ligand-gated ion channels. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. Alternative splicing of this gene results in transcript variants encoding different isoforms, which may vary in their signal transduction properties. Some haplotypes of this gene show a positive association with schizophrenia. Direct phosphorylation of GluR4-containing receptors may regulate rapid excitatory synaptic transmission. In addition, phosphorylation of GluR4 S862. is both necessary and sufficient to deliver the receptor to the synapse and induce plasticity in early postnatal development.
~105 kDa

Immunogen

Synthetic peptide from rat.

Application

Anti-phospho GluR4 (S862) Antibody is an antibody against phospho GluR4 (S862) for use in WB.
Research Category
Neuroscience
Research Sub Category
Neurotransmitters & Receptors
Western Blot Analysis:
Cat. # AB2212 recognizes pGluR4 (S862) at 1:5,000 in rat brain cerebellum Lysate.

Biochem/physiol Actions

Cat. # AB2212 recognzies phospho GluR4 (S862).
May react with mouse, human, primate and dog based on sequence homology. Reactivity with other species has not been tested.

Physical form

Serum with 0.05% NaN3

Preparation Note

Maintain at -20°C in undiluted aliquots for up to 1 year after date of receipt.

Analysis Note

Control
Rat Brain Cerebellum lysate
Routinely tested on rat brain cerebellum lysate.

Legal Information

CHEMICON is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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存储类别

10 - Combustible liquids

wgk

WGK 1


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Pain after discontinuation of morphine treatment is associated with synaptic increase of GluA4-containing AMPAR in the dorsal horn of the spinal cord.
Caba?ero, D; Baker, A; Zhou, S; Hargett, GL; Irie, T; Xia, Y; Beaudry, H; Gendron et al.
Neuropsychopharmacology null

相关内容

Glutamate is an excitatory neurotransmitter found in the synaptic vesicles of glutamatergic synapses. The post-synaptic neurons in these synapses contain ionotropic and metabotropic glutamate receptors. Glutamate binds to AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid) subtype glutamate receptors, leading to sodium influx into the post-synaptic cell and resulting in neuronal excitability and synaptic transmission. The NMDA (N-methyl-d-aspartate) subtype glutamate receptors, on the other hand, regulate synaptic plasticity, and can influence learning and memory. The metabotropic g-protein coupled mGluRs modulate downstream calcium signaling pathways and indirectly influence the synapse’s excitability. The synaptic architecture includes intracellular scaffolding proteins (PSD-95, GRIP), intercellular cell adhesion molecules (NCAMs, N-Cadherins), and a variety of signaling proteins (CaMKII/PKA, PP1/PP2B). Processes critical for synaptic transmission and plasticity are influenced by these molecules and their interactions. When the function of these molecules is disrupted, it leads to synaptic dysfunction and degeneration, and can contribute to dementia as seen in Alzheimer’s disease.

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