Slc13a1 和 Slc26a1 KO 模型揭示阴离子转运体的生理作用。
Slc13a1 and Slc26a1 KO models reveal physiological roles of anion transporters.
机构信息
Molecular Physiology Group, School of Biomedical Sciences, University of Queensland, St. Lucia, Australia.
出版信息
Physiology (Bethesda). 2012 Feb;27(1):7-14. doi: 10.1152/physiol.00041.2011.
Anion transporters NaS1 (SLC13A1) and Sat1 (SLC26A1) mediate sulfate (re)absorption across renal proximal tubule and small intestinal epithelia, thereby regulating blood sulfate levels. Disruption of murine NaS1 and Sat1 genes leads to hyposulfatemia and hypersulfaturia. Sat1-null mice also exhibit hyperoxalemia, hyperoxaluria, and calcium oxalate urolithiasis. This review will highlight the current pathophysiological features of NaS1- and Sat1-null mice resulting from alterations in circulating sulfate and oxalate anion levels.
阴离子转运体 NaS1（SLC13A1）和 Sat1（SLC26A1）介导肾脏近端小管和小肠上皮细胞中的硫酸盐（再）吸收，从而调节血液硫酸盐水平。破坏小鼠的 NaS1 和 Sat1 基因导致低硫酸盐血症和高硫酸盐尿症。Sat1 基因缺失的小鼠还表现出高草酸血症、高草酸尿症和草酸钙尿结石。本综述将重点介绍由于循环硫酸盐和草酸盐阴离子水平的改变，导致 NaS1 和 Sat1 基因缺失的小鼠目前的病理生理学特征。
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