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Previous Volume 349:1401-1404 October 9, 2003 Number 15 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Cystic fibrosis is a heterogeneous condition caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene.¹ The gene product, a regulated chloride channel, is expressed in the apical plasma membrane of secretory and reabsorptive epithelia of affected organs and allows the transepithelial movement of water and solute by mediating chloride translocation across the plasma membrane. Although the mechanism underlying the CFTR-induced regulation of chloride transport activity has largely been elucidated, other effector functions are less well understood.

More than 1000 alterations have been identified in the CFTR gene (for a list, see http://www.genet.sickkids.on.ca/cftr/). Cystic fibrosis . . . [Full Text of this Article]

Source Information

From the Programs in Cell Biology (G.L.L.) and Integrative Biology (P.R.D.), Research Institute, Hospital for Sick Children; and the Departments of Laboratory Medicine and Pathobiology (G.L.L.), Pediatrics (P.R.D.), and Medicine (G.L.L.), University of Toronto — both in Toronto.

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