GRM2
Purified Mouse Monoclonal Antibody
- 产品详情
- 实验流程
Application
| WB, IHC, ICC, E |
|---|---|
| Primary Accession | Q14416 |
| Reactivity | Human |
| Host | Mouse |
| Clonality | Monoclonal |
| Clone Names | 4A10B9 |
| Isotype | Mouse IgG1 |
| Calculated MW | 95568 Da |
| Immunogen | Purified recombinant fragment of human GRM2 (AA: extra 414-558) expressed in E. Coli. |
| Formulation | Purified antibody in PBS with 0.05% sodium azide |
| Gene ID | 2912 |
|---|---|
| Other Names | GLUR2; mGlu2; GPRC1B; MGLUR2 |
| Dilution | WB~~ 1/500 - 1/2000 IHC~~1:100~500 ICC~~N/A E~~ 1/10000 |
| Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | GRM2 is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | GRM2 (HGNC:4594) |
|---|---|
| Synonyms | GPRC1B, MGLUR2 |
| Function | Dimeric G protein-coupled receptor which is activated by the excitatory neurotransmitter L-glutamate (PubMed:37286794). Plays critical roles in modulating synaptic transmission and neuronal excitability. Upon activation by glutamate, inhibits presynaptic calcium channels, reducing further glutamate release and dampening excitatory signaling (By similarity). Mechanistically, ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase. May mediate suppression of neurotransmission or may be involved in synaptogenesis or synaptic stabilization. |
| Cellular Location | Cell membrane; Multi-pass membrane protein. Synapse. Cell projection, dendrite |
| Tissue Location | Detected in brain cortex (at protein level). Widely expressed in different regions of the adult brain as well as in fetal brain. |
Research Areas
For Research Use Only. Not For Use In Diagnostic Procedures.
Application Protocols
Provided below are standard protocols that you may find useful for product applications.
REFERENCES
1.Br J Pharmacol. 2015 May;172(9):2383-96.2.Brain Res. 2009 Jan 16;1249:244-50.
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