SLC23A3 is a renal hypoxanthine transporter
SLC23A3 is a renal hypoxanthine transporter
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DOI：
10.1080/15257770.2022.2028826
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发表时间：
2022-01-11
影响因子：
1.3
通讯作者：
Shibata, Shigeru
中科院分区：
文献类型：
--
作者：
Hosoyamada, Makoto;Tomioka, Naoko H.;Shibata, Shigeru
LLC-PK 1肾细胞显示Na+依赖性和Na+非依赖性次黄嘌呤摄取。而后者被腺嘌呤抑制，两者都不被黄嘌呤抑制。在大鼠中，肠Na+依赖性次黄嘌呤转运蛋白Slc 23 a4在肾脏中不表达，并且其作用被黄嘌呤抑制。本研究的目的是从人肾脏中克隆Slc 23 a4-parabolic SLC 23 A3，并研究其次黄嘌呤转运活性。我们观察到Na+依赖性的10 nM [H-3]-次黄嘌呤摄取SLC 23 A3 RNA注射非洲爪蟾卵母细胞。此外，100 μ M黄嘌呤没有抑制Na+非依赖性300 nM [H-3]-次黄嘌呤摄取，而100 μ M腺嘌呤。这些结果证实了SLC 23 A3是人肾脏中的次黄嘌呤转运蛋白。
LLC-PK1 renal cells show Na+-dependent and Na+-independent hypoxanthine uptake. While the latter is inhibited by adenine, neither are inhibited by xanthine. In rats, intestinal Na+-dependent hypoxanthine transporter Slc23a4 is not expressed in the kidney, and its action is inhibited by xanthine. This study aimed to clone Slc23a4-paralog SLC23A3 from the human kidney and investigate its hypoxanthine transport activity. We observed Na+-dependent 10 nM [H-3]-hypoxanthine uptake in SLC23A3 RNA-injected Xenopus oocytes. Moreover, 100 mu M xanthine did not inhibit Na+-independent 300 nM [H-3]-hypoxanthine uptake, whereas 100 mu M adenine did. These results confirm that SLC23A3 is a hypoxanthine transporter in the human kidney.