Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger

Citation
H. Lohi et al., Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger, GENOMICS, 70(1), 2000, pp. 102-112
Citations number
52
Categorie Soggetti
Molecular Biology & Genetics
Journal title
GENOMICS
ISSN journal
08887543 → ACNP
Volume
70
Issue
1
Year of publication
2000
Pages
102 - 112
Database
ISI
SICI code
0888-7543(20001115)70:1<102:MOFNPA>2.0.ZU;2-L
Abstract
A second distinct family of anion transporters, in addition to the classica l SLC4 (or AE) family, has recently been delineated. Members of the SLC26 f amily are structurally well conserved and can mediate the electroneutral ex change of Cl- for HCO3- across the plasma membrane of mammalian cells like members of the SLC4 family. Three human transporter proteins have been func tionally characterized: SLC26A2 (DTDST), SLC26A3 (CLD or DRA), and SLC26A4 (PDS) can transport with different specificities the chloride, iodine, bica rbonate, oxalate, and hydroxyl anions, whereas SLC26A5 (prestin) was sugges ted to act as the motor protein of the cochlear outer hair cell. We report the expansion of the SLC26 family with five new members in chromosomes 3, 6 , 8, 12, and 17 and mapping of SLC26A1 to 4p16.3. We have characterized one of them, SLC26A6, in more detail. It maps to chromosome 3p21.3, encodes a predicted 738-amino-acid transmembrane protein, and is most abundantly ex p ressed in the kidney and pancreas. Pancreatic ductal cell lines Capan-1 and Capan-2 express SLC26A6, and immunohistochemistry localizes SLC26A6 protei n to the apical surface of pancreatic ductal cells, suggesting it as a cand idate for a luminal anion exchanger. The functional. characterization of th e novel members of this tissue-specific gene family may provide new insight s into anion transport physiology in different parts of the body. (C) 2000 Academic Press.