Figure 1. NECA-induced concentration-dependent stimulation of intracellular calcium mobilization in CHO-K1/ADORA3/Gα15 cells. The cells were loaded with Calcium-4 prior to being stimulated with an ADORA3 receptor agonist, NECA. The intracellular calcium change was measured by FLIPR. The relative fluorescence unit (RFU) were normalized and plotted against the log of the cumulative doses of NECA (Mean ± SEM, n = 3). The EC₅₀ of NECA on this cell was 4.76 nM.
Notes:
1. EC₅₀ value is calculated with four parameter logistic equation:
Y=Bottom + (Top-Bottom)/(1+10^((LogEC₅₀-X)*HillSlope))
X is the logarithm of concentration. Y is the response
Y is RFU and starts at Bottom and goes to Top with a sigmoid shape.
2. Signal to background Ratio (S/B) = Top/Bottom

CHO-K1/ADORA3/Gα15 Stable Cell Line

Extracellular adenosine mediates a multitude of biological effects, including wakefulness, antiarrythmia, bronchoconstriction and response to ischemia and oxidative stress. A family of four G-protein coupled adrenoceptors, A1, A2A, A2B and A3, is responsible for these effects. A3, which couples to Gi/o, is expressed in a wide range of human tissues, but most predominantly in the lung and liver. Recent animal model studies have shown that A3 receptors play important roles in brain ischemia, immunosuppresion, and bronchospasm. A3 receptor agonists and/or agonists may have important clinical value in the treatment of asthma and inflammation. Mice lacking A3 receptors display reduced mast cell degranulation and bronchoconstriction in response to adenosine.

產(chǎn)品編號(hào)	M00464
規(guī)格	2 vials 大單詢價(jià)
數(shù)量
價(jià)格	詢價(jià)


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Description

Extracellular adenosine mediates a multitude of biological effects, including wakefulness, antiarrythmia, bronchoconstriction and response to ischemia and oxidative stress. A family of four G-protein coupled adrenoceptors, A1, A2A, A2B and A3, is responsible for these effects. A3, which couples to G_i/o, is expressed in a wide range of human tissues, but most predominantly in the lung and liver. Recent animal model studies have shown that A3 receptors play important roles in brain ischemia, immunosuppresion, and bronchospasm. A3 receptor agonists and/or agonists may have important clinical value in the treatment of asthma and inflammation. Mice lacking A3 receptors display reduced mast cell degranulation and bronchoconstriction in response to adenosine.

Synonyms

A3 receptor, adenosine A3 receptor, TGPCR1, ARA3, A3AR, A3R, AA3R

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Storage

Liquid nitrogen immediately upon delivery

培養(yǎng)條件

Culture Medium	Ham’s F-12K (Kaighn’s), 10% FBS, 100 μg/ml Hygromycin B (Cat. #10687010, Invitrogen), 8 ug/ml Puromycin (Cat. #A11138-03, Gibco)
Freeze Medium-DATA	45% culture medium, 45% FBS (Cat. #10099-141, Gibco), 10% DMSO (Cat. #D2650, Sigma)

圖例

Figure 1. NECA-induced concentration-dependent stimulation of intracellular calcium mobilization in CHO-K1/ADORA3/Gα15 cells. The cells were loaded with Calcium-4 prior to being stimulated with an ADORA3 receptor agonist, NECA. The intracellular calcium change was measured by FLIPR. The relative fluorescence unit (RFU) were normalized and plotted against the log of the cumulative doses of NECA (Mean ± SEM, n = 3). The EC₅₀ of NECA on this cell was 4.76 nM.
Notes:
1. EC₅₀ value is calculated with four parameter logistic equation:
Y=Bottom + (Top-Bottom)/(1+10^((LogEC₅₀-X)*HillSlope))
X is the logarithm of concentration. Y is the response
Y is RFU and starts at Bottom and goes to Top with a sigmoid shape.
2. Signal to background Ratio (S/B) = Top/Bottom

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CHO-K1/ADORA3/Gα15 Stable Cell Line

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