ADORA2A/Adenosine Receptor A2a (E6M3W) Rabbit mAb #53509
- WB
- F
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 45-60 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Flow Cytometry (Fixed/Permeabilized) | 1:100 - 1:400 |
Storage
Protocol
Specificity / Sensitivity
ADORA2A/Adenosine Receptor A2a (E6M3W) Rabbit mAb recognizes endogenous levels of total ADORA2A/Adenosine Receptor A2a protein. A weak unknown band is detected at 80 kDa in some cell lines.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala405 of human ADORA2A/Adenonsine Receptor A2a protein.
Background
Adenosine Receptor A2a (A2AR) is a G-protein-coupled receptor (GPCR). As a member of the purinergic adenosine receptors (A1, A2, and A3), A2AR activates classic G-protein signaling pathways upon binding of adenosine (1). Adenosine is present in all cells and extracellular fluids. Adenosine signaling, via A2AR, is mobilized during both physiological and pathological conditions. For example, adenosine, via A2AR, modulates neuronal function, acting to fine-tune neuronal function (2). A2AR function is modulated, in part, by its ability to form functional heteromers with other GPCRs, including dopamine receptors (D1 and D3), metabotropic glutamate receptors (mGluR5), and others (3). In the brain, A2AR is enriched in the basal ganglia, suggesting that A2AR may be a potential drug target for neurodegenerative diseases like Parkinson’s disease, drug addiction, and psychiatric disorders (4). Outside of the brain, A2AR may act as an immune checkpoint molecule to maintain an immunosuppressive tumor microenvironment, an environment that exhibits relatively elevated adenosine levels (5,6).
- Le, F. et al. (1996) Biochem Biophys Res Commun 223, 461-7.
- Sulli, G. et al. (2018) Trends Pharmacol Sci 39, 812-27.
- Verzijl, D. and Ijzerman, A.P. (2011) Purinergic Signal 7, 171-92.
- Bogenpohl, J.W. et al. (2012) J Comp Neurol 520, 570-89.
- Menzel, S. et al. (2018) Front Pharmacol 9, 266.
- Leone, R.D. et al. (2015) Comput Struct Biotechnol J 13, 265-72.
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