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Merck
CN

PC246

Anti-GluR1 Rabbit pAb

liquid, Calbiochem®

别名:

Anti-Glutamate Receptor I

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UNSPSC Code:
12352203

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biological source

rabbit

antibody product type

primary antibodies

clone

polyclonal

form

liquid

contains

≤0.1% sodium azide as preservative

species reactivity

rat

manufacturer/tradename

Calbiochem®

storage condition

do not freeze

isotype

IgG

shipped in

wet ice

Quality Level

100

General description

Anti-GluR1, rabbit polyclonal, recognizes the ~105-107 kDa GluR1 in D425 Med cells and hippocampal neurons. Also cross-reacts with a 50 kDa protein in rat brain. It is validated for WB and IF.
Purified rabbit polyclonal antibody. Recognizes the ~105-107 kDa GluR1 protein.
Recognizes the ~105-107 kDa GluR1 protein in D425 Med cells and hippocampal neurons. Also cross-reacts with a 50 kDa protein in rat brain extracts.

Immunogen

a synthetic peptide (RTSDSRDHTRVDWKR) corresponding to amino acids 271-285 of rat GluR1 (numbered from the signal peptide)

Application

Immunoblotting 1-5 µg/ml)

Immunofluorescence (10-20 µg/ml, see application references)

Packaging

Please refer to vial label for lot-specific concentration.

Analysis Note

Positive Control
D425 Med cells, hippocampal neurons

Other Notes

Also recognizes a smaller band at ~50 kDa using whole brain extracts. Immunofluorescence of dissociated cultured rat hippocampal neurons gave a punctate distribution, consistent with previous reports of GluR1 distribution. Antibody should be titrated for optimal results in individual systems.
Zuo, J. et al. 1997. Nature388, 769.
McHugh, T.J., et al. 1996. Cell87, 1339.
Tsien, J.Z., et al. 1996. Cell87, 1327.
Greenamyre, J.T. and Porter, R.H.P. 1994. Neurology44, S7.
Hollmann, M. and Heinemann, S. 1994. Ann. Rev. Neurosci.17, 31.
Bliss, T.V.P. and Collingridge, G.L. 1993. Nature361, 31.
Lomeli, H., et al. 1993. FEBS Lett.315, 318.
Molnar, E. et al. 1993. Neuroscience53, 307.
Advokat, C. and Pellegrin, A.I. 1992. Neurosci. Biobehav. Rev.16, 13.
Beal, M.F. 1992. FASEB J.6, 3338.
Rothman, S.M. 1992. Ann. NY Acad. Sci.648, 132.

Legal Information

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

Disclaimer

Toxicity: Standard Handling (A)

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存储类别

10-13 - German Storage Class 10 to 13

法规信息

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Huong T T Ha et al.
Frontiers in molecular neuroscience, 11, 405-405 (2018-12-14)
During development, pyramidal neurons undergo dynamic regulation of AMPA receptor (AMPAR) subunit composition and density to help drive synaptic plasticity and maturation. These normal developmental changes in AMPARs are particularly vulnerable to risk factors for Autism Spectrum Disorders (ASDs), which
David S Tukey et al.
The Journal of biological chemistry, 288(49), 35297-35306 (2013-10-18)
Regulation of striatal medium spiny neuron synapses underlies forms of motivated behavior and pathological drug seeking. A primary mechanism for increasing synaptic strength is the trafficking of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) into the postsynapse, a process mediated by GluA1 AMPAR
Dhrubajyoti Chowdhury et al.
Frontiers in synaptic neuroscience, 11, 6-6 (2019-03-28)
AMPA-type glutamate receptors (AMPARs) are clustered into functional nanodomains at postsynaptic sites through anchorage by the scaffolding protein, postsynaptic density protein-95 (PSD-95). The synaptic abundance of AMPARs is dynamically controlled in various forms of synaptic plasticity. Removal of AMPARs from
Jessica A Loweth et al.
The European journal of neuroscience, 50(3), 2590-2601 (2018-09-18)
In several brain regions, ongoing metabotropic glutamate receptor 1 (mGlu1) transmission has been shown to tonically suppress synaptic levels of Ca2+ -permeable AMPA receptors (CP-AMPARs) while pharmacological activation of mGlu1 removes CP-AMPARs from these synapses. Consistent with this, we previously
Michael Notaras et al.
Molecular psychiatry, 25(12), 3360-3379 (2019-10-23)
Synaptic plasticity requires a tight control of mRNA levels in dendrites. RNA translation and degradation pathways have been recently linked to neurodevelopmental and neuropsychiatric diseases, suggesting a role for RNA regulation in synaptic plasticity and cognition. While the local translation
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Pathways and Biomarkers of Glutamatergic Synapse Flyer

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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