Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Ishiguro, H. et al.

Ishiguro, Namkung, Yamamoto, Wang, Worrell, Xu, Lee, Soleimani,

Effect of Slc26a6 deletion on apical Cl-/HCO3- exchanger activity and cAMP-stimulated bicarbonate secretion in pancreatic duct.

The role of Slc26a6 ( PAT1) on apical Cl(-)/HCO(3)(-) exchange and bicarbonate secretion in pancreatic duct cells was investigated using Slc26a6 null and wild-type (WT) mice. Apical Cl(-)/HCO(3)(-) exchange activity was measured with the pH-sensitive dye BCECF in microperfused interlobular ducts. The HCO(3)(-)-influx mode of apical [Cl(-)](i)/[HCO(3)(-)](o) exchange (where brackets denote concentration and subscripts i and o denote intra- and extracellular, respectively) was dramatically upregulated in Slc26a6 null mice (P < 0.01 vs. WT), whereas the HCO(3)(-)-efflux mode of apical [Cl(-)](o)/[HCO(3)(-)](i) exchange was decreased in Slc26a6 null mice (P < 0.05 vs. WT), suggesting the unidirectionality of the Slc26a6-mediated HCO(3)(-) transport. Fluid secretory rate in interlobular ducts were comparable in WT and Slc26a6 null mice (P > 0.05). In addition, when pancreatic juice was collected from whole animal in basal and secretin-stimulated conditions, neither juice volume nor its pH showed differences between WT and Slc26a6 null mice. Semiquantitative RT-PCR demonstrated more than fivefold upregulation in Slc26a3 (DRA) expression in Slc26a6 knockout pancreas. In conclusion, these results point to the role of Slc26a6 in HCO(3)(-) efflux at the apical membrane and also suggest the presence of a robust Slc26a3 compensatory upregulation, which can replace the function of Slc26a6 in pancreatic ducts.[1]

References

Effect of Slc26a6 deletion on apical Cl-/HCO3- exchanger activity and cAMP-stimulated bicarbonate secretion in pancreatic duct. Ishiguro, H., Namkung, W., Yamamoto, A., Wang, Z., Worrell, R.T., Xu, J., Lee, M.G., Soleimani, M. Am. J. Physiol. Gastrointest. Liver Physiol. (2007) [Pubmed]

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