Projects per year
One therapeutic strategy for cystic fibrosis (CF) seeks to restore anion transport to affected epithelia by targeting other apical membrane Cl(-) channels to bypass dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel. The properties and regulation of the Ca(2+)-activated Cl(-) channel TMEM16A argue that long-acting small molecules which target directly TMEM16A are required to overcome CFTR loss. Through genetic studies of lung diseases, SLC26A9, a member of the solute carrier 26 family of anion transporters, has emerged as a promising target to bypass CFTR dysfunction. An alternative strategy to circumvent CFTR dysfunction is to deliver to CF epithelia artificial anion transporters that shuttle Cl(-) across the apical membrane. Recently, powerful, non-toxic, biologically-active artificial anion transporters have emerged.
Bibliographical noteIssue cover date: June 2017
10/09/12 → 9/03/16
1/11/08 → 1/03/12