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. Footnotes This work was supported in part by the Australian Research Council, National Health and Medical Research Council, and Cancer Council Queensland. No conflicts of interest, financial or otherwise, are declared by the author(s). Author contributions: D.M. conception and design of research; D.M. performed experiments; D.M. analyzed data; D.M. interpreted results of experiments; D.M. prepared figures; D.M. drafted the manuscript; D.M. edited and revised the manuscript; D.M. approved the final version of the manuscript. ©2012 Int. Union Physiol. Sci./Am. Physiol. Soc. « Previous | Next Article » Table of Contents This Article doi: 10.1152/physiol.00041.2011 Physiology February 2012 vol. 27 no. 1 7-14 » Abstract Free Full Text Free to you Full Text (PDF) Free to you Classifications Review Services Email this article to a friend Alert me when this article is cited Alert me if a correction is posted Similar articles in this journal Similar articles in Web of Science Download to citation manager Citing Articles Load citing article information Citing articles via Web of Science Google Scholar Articles by Markovich, D. PubMed Articles by Markovich, D. Related Content Load related web page information Current Issue February 2012, 27 (1) Alert me to new issues of Physiology About the Journal Information for Authors Submit a Manuscript Ethical Policies AuthorChoice PubMed Central Policy Reprints and Permissions Advertising Press Copyright © 2012 the American Physiological Society Print ISSN: 1548-9213 Online ISSN: 1548-9221 var gaJsHost = (("https:" == document.location.protocol) ? "https://ssl." : "http://www."); document.write(unescape("%3Cscript src='" + gaJsHost + "google-analytics.com/ga.js' type='text/javascript'%3E%3C/script%3E")); var pageTracker = _gat._getTracker("UA-2924550-1"); pageTracker._trackPageview();
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