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Bicarbonate transport in cystic fibrosis.
Supported by the Canadian Cystic Fibrosis Foundation.

Abnormal Cl- secretion is well characterized in cystic fibrosis (CF).  Less well appreciated is that normal pancreatic secretion of 140 mM HCO3- is frequently disrupted in CF patients and that loss of HCO3- secretion capacity correlates strongly with disease severity in CF, even more strongly than with epithelial Cl- conductance.  Although the basis for the HCO3- secretion defect in CF is not well understood, it is now appreciated as an important area of study.  This led to our studies of the regulation of transport by SLC26A6, a Cl-/HCO3- exchanger expressed on the apical surface of pancreatic ducts.  We are presently examining the roles and regulation of bicarbonate transporters in tissues affected by CF.




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