OXGR1, i.e., 2-oxoglutarate receptor 1 (also known as GPR99, cysteinyl leukotriene receptor E, i.e., CysLTE, and cysteinyl leukotriene receptor 3, i.e., CysLT3[5][6]) is a G protein-coupled receptor located on the surface membranes of certain cells. It functions by binding one of its ligands and thereby becoming active in triggering pre-programmed responses in its parent cells. OXGR1 has been shown to be activated by α-ketoglutarate,[7] itaconate,[8] and three cysteinyl-containing leukotrienes (abbreviated as CysLTs), leukotriene E4 (i.e., LTE4), LTC4, and LTD4.[5][9] α-Ketoglutarate and itaconate are the dianionic forms of α-ketoglutaric acid and itaconic acid, respectively. α-Ketoglutaric and itaconic acids are short-chain dicarboxylic acids that have two carboxyl groups (notated as -CO2H) both of which are bound to hydrogen (i.e., H+). However, at the basicpH levels (i.e., pH>7) in virtually all animal tissues, α-ketoglutaric acid and itaconic acid exit almost exclusively as α-ketoglutarate and itaconate, i.e., with their carboxy residues being negatively charged (notated as -CO2), because they are not bound to H+ (see Conjugate acid-base theory). It is α-ketoglutarate and itaconate, not α-ketoglutaric or itaconic acids, which activate OXGR1.[7][8]
^Yamamoto T, Miyata J, Arita M, Fukunaga K, Kawana A (November 2019). "Current state and future prospect of the therapeutic strategy targeting cysteinyl leukotriene metabolism in asthma". Respiratory Investigation. 57 (6): 534–543. doi:10.1016/j.resinv.2019.08.003. PMID31591069.
^ abGrimm PR, Welling PA (September 2017). "α-Ketoglutarate drives electroneutral NaCl reabsorption in intercalated cells by activating a G-protein coupled receptor, Oxgr1". Current Opinion in Nephrology and Hypertension. 26 (5): 426–433. doi:10.1097/MNH.0000000000000353. PMID28771454.
^Sasaki F, Yokomizo T (August 2019). "The leukotriene receptors as therapeutic targets of inflammatory diseases". International Immunology. 31 (9): 607–615. doi:10.1093/intimm/dxz044. PMID31135881.
