MABN139
Anti-mGluR5 Antibody, clone 11D9.1
clone 11D9.1, from mouse
Synonym(s):
Metabotropic glutamate receptor 5, mGluR5
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About This Item
biological source
mouse
Quality Level
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
11D9.1, monoclonal
species reactivity
human, rat
technique(s)
immunohistochemistry: suitable
western blot: suitable
isotype
IgG2bκ
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... GRM5(2915)
General description
Immunogen
Application
Physical form
Analysis Note
Rat brain micropreparation tissue lysate
Western Blotting Analysis: 1.0 µg/mL of this antibody detected mGluR5 in 10 µg of rat brain micropreparation tissue lysate. The lysate was not boiled during preperation for western blotting.
Other Notes
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Storage Class
12 - Non 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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