Slc13a1 and Slc26a1 KO models reveal physiological roles of anion transporters.
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.
Molecular Physiology Group, School of Biomedical Sciences, University of Queensland, St. Lucia, Australia. d.markovich@uq.edu.au
Daniel
D
Markovich
D000818:Animals; D027321:Anion Transport Proteins / Q000235:genetics* / Q000378:metabolism*; D055786:Gene Knockout Techniques / Q000379:methods; D006801:Humans; D010070:Oxalates / Q000378:metabolism; D013431:Sulfates / Q000378:metabolism
D027321:Anion Transport Proteins; D010070:Oxalates; D013431:Sulfates