Presentation: P03012

The Complement system is central to innate immunity and a variety of inflammatory responses. C3a is a byproduct of complement activation which activates mast cells, basophils and eosinophils driving smooth muscle contraction and, as such, is thought to play a role in the pathogenesis of allergic asthma (Ali & Panettieri). We have developed a FLIPR-based functional assay for C3a receptor activation by utilizing a dual BacMam transfection of C3a receptor and the promiscuous G-protein Gα 16. The potential for fine tuning expression levels and receptor:G-protein stoichiometry under the BacMam transfection system affords us the opportunity to calibrate in vitro functional responses such that they more closely reflect the pharmacology in native expression systems. This methodology also affords the possibility of rapid, high-throughput screening of the C3a receptor via signaling coupled to a Ca²⁺ read-out, whilst retaining appropriate agonist pharmacology.

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