MAB1586
Anti-NMDAR1 Antibody, (all splice variants), clone R1JHL
clone R1JHL, Chemicon®, from mouse
Synonym(s):
Anti-GluN1, Anti-NDHMSD, Anti-NDHMSR, Anti-NMD-R1, Anti-NMDA1, Anti-NMDAR1, Anti-NR1
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About This Item
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
affinity purified immunoglobulin
antibody product type
primary antibodies
clone
R1JHL, monoclonal
species reactivity
mouse, rat, human
manufacturer/tradename
Chemicon®
technique(s)
western blot: suitable
isotype
Not specified
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Gene Information
human ... GRIN1(2902)
mouse ... Grin1(14810)
rat ... Grin1(24408)
Immunogen
Application
Neuroscience
Neurotransmitters & Receptors
Immunoprecipitation: 3 μg per 200 μg of lysate will quantitatively precipitate all the NMDA R1 in 200 μg of rat brain lysate.
Optimal working dilutions must be determined by end user.
Biochem/physiol Actions
Physical form
Preparation Note
Legal Information
Disclaimer
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Storage Class
10 - Combustible liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
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Related Content
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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