SLC17A3-2 transports cytosolic urate to extracellular region

Stable Identifier
Reaction [transition]
Homo sapiens
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Human serum urate levels are largely maintained by its reabsorption and secretion in the kidney. Loss of this maintenance can elevate urate levels leading to gout, hypertension, and various cardiovascular diseases. Renal urate reabsorption is controlled via two proximal tubular urate transporters; apical SLC22A12 (URAT1) and basolateral SLC2A9 (URATv1, GLUT9). On the other hand, urate secretion is mediated by the orphan sodium phosphate transporter 4 isoform 2 (SLC17A3, NPT4 isoform 2). It is mainly expressed at the apical side of renal tubules and functions as a voltage-driven urate transporter (Jutabha et al. 2010).

Genetic variations in SLC17A3 influence the variance in serum uric acid concentrations and define the serum uric acid concentration quantitative trait locus 4 (UAQTL4; MIM:612671). Excess serum urate (hyperuricemia) can lead to the development of gout, characterized by tissue deposition of monosodium urate crystals.
Literature References
PubMed ID Title Journal Year
20810651 Human sodium phosphate transporter 4 (hNPT4/SLC17A3) as a common renal secretory pathway for drugs and urate

Wempe, MF, Katada, T, Kimura, T, Fujita, T, Sakurai, H, Yamada, A, Shimada, H, Uchida, S, Yamanaka, H, Tomita, K, Endou, H, Yan, K, Jutabha, P, Fukutomi, T, Kitamura, K, Anzai, N, Urano, W, Seki, G, Taniguchi, A, Yamada, H, Moriyama, Y, Kaneko, S

J. Biol. Chem. 2010
Catalyst Activity

urate transmembrane transporter activity of SLC17A3(1-498) [plasma membrane]

Orthologous Events
Cross References
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