title: Physiological roles of renal anion transporters NaS1 and Sat1.
abstract: This review will briefly summarize current knowledge on the renal anion transporters sodium-sulfate cotransporter-1 (NaS1; Slc13a1) and sulfate-anion transporter-1 (Sat1; Slc26a1). NaS1 and Sat1 mediate renal proximal tubular sulfate reabsorption and thereby regulate blood sulfate levels. Sat1 also mediates renal oxalate transport and controls blood oxalate levels. Targeted disruption of murine NaS1 and Sat1 leads to hyposulfatemia and hypersulfaturia. Sat1 null mice also exhibit hyperoxalemia, hyperoxaluria, and calcium oxalate urolithiasis. NaS1 and Sat1 null mice also have other phenotypes that result due to changes in blood sulfate and oxalate levels. Experimental data indicate that NaS1 is essential for maintaining sulfate homeostasis, whereas Sat1 controls both sulfate and oxalate homeostasis in vivo.
authors.affiliation: Molecular Physiology Group, School of Biomedical Sciences, Univ. of Queensland, St. Lucia, Australia. d.markovich@uq.edu.au
authors.forename: Daniel
authors.initials: D
authors.lastname: Markovich
mesh_terms: D000818:Animals; D027321:Anion Transport Proteins / Q000378:metabolism*; D027682:Cation Transport Proteins / Q000378:metabolism*; D017136:Ion Transport / Q000502:physiology; D007668:Kidney / Q000378:metabolism*; D051379:Mice; D018345:Mice, Knockout; D000077003:Sodium Sulfate Cotransporter; D027981:Symporters / Q000378:metabolism*
chemical_list: D027321:Anion Transport Proteins; D027682:Cation Transport Proteins; D000077003:Sodium Sulfate Cotransporter; D027981:Symporters