Metabotropic Glutamate Receptor 5 (GRM5) Rabbit Monoclonal Antibody [Clone ID: EPR2425Y]

CAT#: TA301102

Rabbit Monoclonal Antibody against GRM5 (Clone EPR2425Y)


USD 531.00

In Stock*

Size
    • 100 ul

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Specifications

Product Data
Clone Name EPR2425Y
Applications IHC, WB
Recommended Dilution WB: 1:5000; IHC: 1:250; ICC: 1: 100; FC: 1: 10
Reactivities Human, Mouse, Rat
Host Rabbit
Isotype IgG
Clonality Monoclonal
Immunogen A synthetic peptide corresponding to residues near the C-terminus of human mGluR5
Formulation PBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%
Purification Tissue culture supernatant
Conjugation Unconjugated
Storage Store at -20°C as received.
Stability Stable for 12 months from date of receipt.
Predicted Protein Size 132 kDa
Gene Name glutamate metabotropic receptor 5
Background L-glutamate is the major excitatory neurotransmitter in the central nervous system and activates both ionotropic and metabotropic glutamate receptors. Class I metabotropic glutamate receptors (mGluRs) have been postulated to play a role in synaptic plasticity. It has been suggested that mGluR5 may be the primary high affinity ACPD receptor in CA1 neurons (1). Also, neuroprotection by mGluR system has been linked to the modulation of both the free radical nitric oxide (NO) and programmed cell death (PCD). Activation of group I mGluR subtypes utilized an effective, "upstream" mechanism for the inhibition of cysteine protease activity that offered an enhanced level of neuroprotection through both the preservation of genomic DNA integrity and the maintenance of PS membrane asymmetry (2). It has also been shown that activation of mGluRs enhances formation of an mGluR-Homer-PIKE-L complex, leading to activation of PI3 kinase activity and prevention of neuronal apoptosis. Our findings indicate that this complex mediates the well-known ability of agonists of mGluR5 to prevent neuronal apoptosis (3).
Synonyms GPRC1E; mGlu5; MGLUR5; PPP1R86
Reference Data
Protein Families Druggable Genome, GPCR, Transmembrane
Protein Pathways Calcium signaling pathway, Gap junction, Huntington's disease, Long-term depression, Long-term potentiation, Neuroactive ligand-receptor interaction

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