T-cell death-associated gene 8 (TDAG8) functions as a proton sensing GPCR. TDAG8 was originally proposed to bind pro-inflammatory lipids. More recent studies have challenged the identification of lipid agonists for TDAG8 and have suggested that it functions mainly as a proton sensor.
Researchers at UCLA have developed a mouse model deficient for TDAG8. It was confirm by using this model that the inactivation of TDAG8 proton sensor abolishes acid-induced production of the secondary messenger cyclic AMP in immune cells.
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