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A2AR Protein-VLP, Human, Recombinant (Flag)

Catalog No. TMPY-07100

A2AR Protein-VLP, Human, Recombinant (Flag) is expressed in HEK293 Cells. The accession number is P29274.

A2AR Protein-VLP, Human, Recombinant (Flag)

A2AR Protein-VLP, Human, Recombinant (Flag)

Catalog No. TMPY-07100
A2AR Protein-VLP, Human, Recombinant (Flag) is expressed in HEK293 Cells. The accession number is P29274.
Pack SizePriceAvailabilityQuantity
20 μg$983Backorder
100 μg$2,080Backorder
500 μg$7,450Backorder
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Product Information

Biological Activity
Immobilized A2AR Protein-VLP, Human, Recombinant (Flag) (Cat#TMPY-07100) at 5 μg/mL (100 μL/well) can bind Anti-Human ADORA2A Monoclonal antibody, Mouse IgG2a, the EC50 is 5-20 ng/mL.
Description
A2AR Protein-VLP, Human, Recombinant (Flag) is expressed in HEK293 Cells. The accession number is P29274.
Species
Human
Expression System
HEK293 Cells
TagN-Flag
Accession NumberP29274
Construction
A DNA sequence encoding the Human AA2AR (P29274) (Met1-Ser412) was expressed with a flag tag at the N-terminus.
Molecular Weight38.06 kDa (predicted)
Endotoxin< 1.0 EU per μg of the protein as determined by the LAL method
FormulationSupplied as sterile 50 mM Hepes, 150 mM NaCl, 10% Trehalose, pH 7.2. Please contact us for any concerns or special requirements. Please refer to the specific buffer information in the hardcopy of datasheet or the lot-specific COA.
Stability & Storage
Samples are stable for up to twelve months from date of receipt at -70℃. Store it under sterile conditions at -70℃ or lower. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
ShippingIt is supplied and shipped as liquid with dry ice.
Research Background
Adenosine Receptor Subtype A2a (A2aR) is a G-protein coupled receptor that mediates adenosine (a potent immunosuppressor) signaling in leukocytes. A2aR has been implicated in neuroinflammation and synaptic plasticity-related processes. Signaling through A2aRs inhibits local and systemic inflammation and A2aR expression showed protective effects against non-alcoholic steatohepatitis (NASH) in the liver. A2aR deficiency triggers spontaneous inflammation and NASH-Hepatocellular Carcinoma (HCC) in mice while low A2aR gene expression in human HCC is associated with hepatic inflammation and poor survival. Reducing adenosine signaling via A2aR antagonism provides an alternative targeted strategy to modulate the number and efficacy of infiltrating effector T cells within the immunosuppressive tumor microenvironment. Co-blockade of A2aR signaling and CD73 reduced tumor initiation, growth, and metastasis.

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