Adenosine A2a receptor (A2aR or ADORA2A) stably expressed in HEK-293 cells. A2aR is a member of the seven transmembrane G protein-coupled receptor (GPCR) family. The activity of A2aR is mediated by G?s protein which activates adenylyl cyclase, resulting in the synthesis of intracellular cAMP. The level of cAMP correlates with the respective adenosine (agonist) level, and the cell line can be used to measure the EC50 and IC50 values of A2aR agonists or antagonists in a quantitative manner. Binding of extracellular adenosine ligand or its stable analog NECA (5 -(N-Ethylcarboxamido) adenosine) to the A2aR expressed on the surface of this cell line induces cAMP expression.
Mycoplasma testing: This cell line has been screened using the MycoAlert Mycoplasma Detection Kit (Lonza, #LT07-118) to confirm the absence of Mycoplasma contamination. MycoAlert Assay Control Set (Lonza, #LT07-518) was used as a positive control.
Host Species: human
Supplied as Each vial contains ~ 2 x 106 cells in 1 ml of 10% DMSO in FBS.
Background
Adenosine signaling plays an important role in inflammation and the immune response. Many cells in the tumor microenvironment express ectopic CD39 and CD73, leading to the buildup of extracellular adenosine. Engagement of adenosine with the high affinity A2a receptor (A2aR) on the surface of T cells, macrophages, NK cells, neutrophils, and dendritic cells causes downregulation of the immune response. Therefore, A2aR is a novel immune checkpoint protein, and blockade of A2aR is being actively investigated as a potential immunotherapy. Several A2aR antagonists have progressed to clinical trials for the treatment of Parkinson's disease, and preclinical studies have confirmed that blockade of A2a receptor activation has the ability to markedly enhance anti-tumor immunity. Mice treated with A2aR antagonists, such as ZM241385 (see data below) or caffeine, show significantly delayed tumor growth, and A2aR knockout mice demonstrate increased tumor rejection. Most promising, A2aR blockade can be used in synergy with the inhibition of other immune checkpoint pathways. Studies show that the combination of A2aR blockade and PD-1 inhibition is more effective than either treatment separately, and A2aR blockade increases the activity of CTLA-4 and TIM-3 inhibition in controlling the growth of CD73+ melanoma.
Application
Screen for agonists or antagonists of A2aR in cell-based cAMP assays. Study PD-1 and CTLA-4 combination therapy. Screen co-inhibitor immune checkpoint molecules for cancer immunotherapy.
Host Cell
HEK293
Synonyms
A2aR, ADORA2A
Shipping Temperature
-80°C (dry ice)
Note
License Disclosure: Purchase of this cell line grants you with a 10-year license to use this cell line in your immediate laboratory, for research use only. This license does not permit you to share, distribute, sell, sublicense, or otherwise make the cell line available for use to other laboratories, departments, research institutions, hospitals, universities, or biotech companies. The license does not permit the use of this cell line in humans or for therapeutic or drug use. The license does not permit modification of the cell line in any way. Inappropriate use or distribution of this cell line will result in revocation of the license and result in an immediate cease of sales and distribution of Biohippo products to your laboratory. Biohippo does not warrant the suitability of the cell line for any particular use, and does not accept any liability in connection with the handling or use of the cell line. Modifications of this cell line, transfer to another facility, or commercial use of the cells may require a separate license and additional fees; contact [email protected] for details. Publications using this cell line should reference Biohippo Inc. Warning: Avoid freeze/thaw cycles.
Storage Stability
Immediately upon receipt, store in liquid nitrogen.
Reference
1. Leone, R.D., et.al. (2015). Comp. Struct. Biotechnol. J. 13: 265-2722. Ma, S-R., et al. (2017). Molec. Cancer 16:993. Ohta, A., et al. (2016). Front. Immunol. 7:109.