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J. Biol. Chem., Vol. 280, Issue 8, 6463-6470, February 25, 2005
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SLC26A7 Is a Cl– Channel Regulated by Intracellular pH*
From the Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9040
Members of the SLC26 transporter family play an essential role in several epithelial functions, as revealed by diseases associated with mutations in members of the family. Several members were shown to function as Cl– and 
transporters that likely play an important role in epithelial Cl– absorption and secretion. However, the mechanism of most transporters is not well understood. SLC26A7 is a member of the SLC26 transporter family reported to be expressed in the basolateral membrane of the cortical collecting duct and parietal cells and functions as a coupled 
exchanger. In the present work we examined the transport properties of SLC26A7 to determine its transport characteristics and electrogenicity. We found that when expressed in Xenopus oocytes or HEK293 cells SLC26A7 functions as a pHi-regulated Cl– channel with minimal 
permeability. Expression of SLC26A7 in oocytes or HEK293 cells generated a Cl– current with linear I/V and an instantaneous current that was voltage- and time-independent. Based on measurement of reversal potential the selectivity of SLC26A7 is 
, although I– partially inhibited the current. Incubating the cells with or butyrate acidified the cytosol and increased the selectivity of SLC26A7 for Cl–. Measurement of membrane potential and pHi showed minimal OH– and transport by SLC26A7 when the cells were incubated in Cl–-containing or Cl–-free media. The activity of SLC26A7 was inhibited by all inhibitors of anion transporters tested, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, diphenylamine-2-carboxylic acid, and glybenclamide. These findings reveal that SLC26A7 functions as a unique Cl– channel that is regulated by intracellular H+.
Received for publication, August 10, 2004 , and in revised form, December 8, 2004.
* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Both authors contributed equally to this work.
To whom correspondence should be addressed: Dept. of Physiology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd., Dallas, TX 75390-9040. Tel.: 214-648-2593; Fax: 214-648-8974; E-mail: shmuel.muallem{at}utsouthwestern.edu.
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