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Merck
CN

07-258

Anti-GluR5 Antibody

Upstate®, from rabbit

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关于此项目

UNSPSC Code:
12352203
NACRES:
NA.41
eCl@ss:
32160702
Conjugate:
unconjugated
Clone:
polyclonal
Application:
western blot
Species reactivity:
rat
Citations:
3
Technique(s):
western blot: suitable
Uniprot accession no.:
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产品名称

Anti-GluR5 Antibody, Upstate®, from rabbit

biological source

rabbit

conjugate

unconjugated

antibody form

purified antibody

antibody product type

primary antibodies

clone

polyclonal

species reactivity

rat

manufacturer/tradename

Upstate®

technique(s)

western blot: suitable

isotype

IgG

NCBI accession no.

UniProt accession no.

shipped in

dry ice

target post-translational modification

unmodified

Quality Level

Gene Information

human ... GRIK1(2897)

Analysis Note

routinely evaluated by immunoblot on RIPA lysates from a rat brain microsomal preparation

Application

Anti-GluR5 Antibody is an antibody against GluR5 for use in WB.
Research Category
Neuroscience
Research Sub Category
Neurotransmitters & Receptors

Neurodegenerative Diseases

Biochem/physiol Actions

GluR5 isoforms

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.

General description

105-110kDa

Immunogen

peptide corresponding to amino acids 937-949 (CHQRRTQRKETVA) of rat GluR5-2C isoform precursor

Physical form

0.1M Tris-glycine, pH 7.4, 0.15M NaCl, 0.05% sodium azide before the addition of glycerol to 30%
Format: Purified
Protein A chromatography

Preparation Note

2 years at -20°C

Legal Information

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

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存储类别

10 - Combustible liquids

wgk

WGK 2


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Gui-Fang Duan et al.
Nature communications, 9(1), 4879-4879 (2018-11-20)
Kainate-type glutamate receptors play critical roles in excitatory synaptic transmission and synaptic plasticity in the brain. GluK1 and GluK2 possess fundamentally different capabilities in surface trafficking as well as synaptic targeting in hippocampal CA1 neurons. Here we find that the
Scott E Hemby et al.
Journal of neurochemistry, 95(6), 1785-1793 (2005-12-21)
Chronic cocaine and withdrawal induce significant alterations in nucleus accumbens (NAc) glutamatergic function in humans and rodent models of cocaine addiction. Dysregulation of glutamatergic function of the prefrontal cortical-NAc pathway has been proposed as a critical substrate for unmanageable drug
Shuang Qiu et al.
Molecular brain, 11(1), 54-54 (2018-09-23)
Fragile X syndrome is caused by the loss of fragile X mental retardation protein (FMRP). Kainate receptor (KAR) is a subfamily of ionotropic glutamate receptors (iGluR) that acts mainly as a neuromodulator of synaptic transmission and neuronal excitability. However, little

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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