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Cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene that encodes a small conductance cAMP-activated chloride ion channel. In the CF pancreatic duct, mutations in CFTR cause a reduction in bicarbonate secretion. This is thought to result from CFTR operating in parallel with a chloride-bicarbonate (Cl(-)/HCO(-)(3)) exchanger, located in the apical membrane of pancreatic duct cells. The molecular basis of this Cl(-)/HCO(-)(3) exchanger has not been identified. A combination of screening cDNA libraries, RNase protection, and 5' RACE analysis was used to identify Cl(-)/HCO(-)(3) exchangers in human fetal pancreas. An AE2 Cl(-)/HCO(-)(3) exchanger was shown to be expressed in human fetal pancreas from the midtrimester of gestation, at a time when CF-associated pathology commences. In addition, an AE1 Cl(-)/HCO(3) was identified in fetal pancreas but was absent from the adult pancreas and cultured ductal epithelial cells from fetal and adult pancreas.

Original publication




Journal article


Biochem Biophys Res Commun

Publication Date





315 - 321


Adult, Anion Exchange Protein 1, Erythrocyte, Anion Transport Proteins, Antiporters, Base Sequence, Bicarbonates, Chloride-Bicarbonate Antiporters, Chlorides, Cystic Fibrosis Transmembrane Conductance Regulator, DNA, Complementary, Fetus, Gene Library, Humans, Membrane Proteins, Molecular Sequence Data, Pancreatic Ducts, SLC4A Proteins