Scientific background:

Summary: The gene product of the SLC26A6 is an oxalate transporter. Mutations in this gene are probably responsible for nephrolithiasis that is associatedwith chronic diarrhea.

Methodology:

Literature: 

Chernova MN et al. (2005) Functional comparison of mouse slc26a6 anion exchanger with human SLC26A6 polypeptide variants: differences in anion selectivity, regulation, and electrogenicity.
Jiang Z et al. (2006) Calcium oxalate urolithiasis in mice lacking anion transporter Slc26a6.
Kleta R et al. (2006) A key stone cop regulates oxalate homeostasis.
Lohi H et al. (2000) Mapping of five new putative anion transporter genes in human and characterization of SLC26A6, a candidate gene for pancreatic anion exchanger.
Waldegger S et al. (2001) Cloning and characterization of SLC26A6, a novel member of the solute carrier 26 gene family.
Sakhaee K et al. (2009) Recent advances in the pathophysiology of nephrolithiasis.
Sindic A et al. (2007) Renal physiology of SLC26 anion exchangers.
Kere J et al. (2006) Overview of the SLC26 family and associated diseases.
Soleimani M et al. (2006) SLC26 chloride/base exchangers in the kidney in health and disease.
Markovich D et al. (2007) Specificity and regulation of renal sulfate transporters.