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Solute carrier family 2, facilitated glucose transporter member 9 (SLC2A9, also known as GLUT9), is a high-capacity urate transporter primarily expressed in the renal proximal tubules and other tissues[3][4][6]. Although initially identified due to its homology with glucose transporters, SLC2A9 has a strong preference for urate over glucose and fructose, acting as the main pathway for returning urate from renal tubular cells to plasma and thus regulating serum uric acid levels[1][2][3][4]. Mutations or alterations in SLC2A9 expression can result in either hypouricemia (with risk of kidney stones and exercise-induced symptoms) or hyperuricemia (predisposing to gout and nephrolithiasis)[5]. Recent structural studies have detailed the substrate-binding mode, revealed how certain inhibitors such as apigenin can block urate transport, and highlighted the role of disease-associated mutations in transporter function—making SLC2A9 a promising therapeutic target for diseases of uric acid dysregulation, most notably gout and related disorders[1][2][4].
Inhibitors block urate binding/transport through competitive occupation of the substrate binding site or allosteric modulation[1] Modulating SLC2A9 activity alters plasma uric acid concentration by influencing renal reabsorption and efflux of urate[2][4][5]
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