G8913
Anti-Glutamate Receptor NMDAR1 (NR1) antibody produced in rabbit
affinity isolated antibody, buffered aqueous solution
Synonym(s):
Anti-GluN1, Anti-MRD8, Anti-NDHMSD, Anti-NDHMSR, Anti-NMD-R1, Anti-NMDA1, Anti-NMDAR1, Anti-NR1
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About This Item
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biological source
rabbit
Quality Level
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 116 kDa
species reactivity
rat, human, mouse
packaging
antibody small pack of 25 μL
General description
N-methyl-D-aspartate receptors (NMDAR1) is mainly expressed in mammalian brain. The gene is located on human chromosome 9q34.3.
NMDAR1 is a subunit of N-methyl D-aspartate (NMDA) receptor which is a subtype of glutamate-gated ion channels with high calcium permeability. NMDA receptors have unique voltage-dependent sensitivity to magnesium and are modified by glycine. It has a pivotal role in neuronal development, pathogenesis of acute and chronic neurodegenerative disorders, synaptic plasticity as well as memory acquisition and learning. Anti-glutamate receptor NMDAR1 (NR1) antibody can be used for studying the expression and function of NMDAR1 in different cell types and tissues as well as to compare its expression pattern with physiological functions or pathological conditions. Rabbit anti-glutamate receptor NMDAR1 (NR1) antibody reacts specifically with NMDAR1 (116kD) derived from rat brain.
Immunogen
synthetic peptide corresponding to the C-terminal region of rat NMDAR1 (amino acids 918-938). This sequence is identical in mouse NR1, human NR1 (short and long forms), and rat NR1 isoforms NR1b, NR1c, and NR1f.
Application
Anti-Glutamate Receptor NMDAR1 (NR1) antibody produced in rabbit has been used in endogenous calmodulin co-immunoprecipitation and immunoprecipitation.
Anti-glutamate receptor NMDAR1 (NR1) antibody can be used as a primary antibody in western blotting. It can also be used to identify NR1 from rat brain synaptosomal fraction by using immunoblotting.
Biochem/physiol Actions
N-methyl-D-aspartate receptor1 (NMDAR1) regulates excitatory synaptic transmission. Abnormal functioning of this receptor is associated with epilepsy and schizophrenia.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 1% BSA and 15 mM sodium azide.
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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Storage Class
12 - Non Combustible Liquids
wgk_germany
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
ppe
Eyeshields, Gloves, multi-purpose combination respirator cartridge (US)
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Diego Peretti et al.
Nature, 518(7538), 236-239 (2015-01-22)
In the healthy adult brain synapses are continuously remodelled through a process of elimination and formation known as structural plasticity. Reduction in synapse number is a consistent early feature of neurodegenerative diseases, suggesting deficient compensatory mechanisms. Although much is known
Mutation analysis of the N-methyl-D-aspartate receptor NR1 subunit gene (GRIN1) in schizophrenia
Sakurai K, et al.
Neuroscience Letters, 296(2-3), 168-170 (2000)
Single amino acid residue in the M4 domain of GluN1 subunit regulates the surface delivery of NMDA receptors
Kaniakova M, et al.
Journal of Neurochemistry, 123(3), 385-395 (2012)
Jesús Planagumà et al.
Annals of neurology, 80(3), 388-400 (2016-07-12)
To demonstrate that ephrin-B2 (the ligand of EphB2 receptor) antagonizes the pathogenic effects of patients' N-methyl-D-aspartate receptor (NMDAR) antibodies on memory and synaptic plasticity. One hundred twenty-two C57BL/6J mice infused with cerebrospinal fluid (CSF) from patients with anti-NMDAR encephalitis or
Ephrin-B2 prevents N-methyl-D-aspartate receptor antibody effects on memory and neuroplasticity
Planaguma J, et al.
Annals of Neurology, 80(3), 388-400 (2016)
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