期刊
CURRENT OPINION IN PHARMACOLOGY
卷 34, 期 -, 页码 91-97出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.coph.2017.10.002
关键词
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资金
- Engineering and Physical Sciences Research Council [EP/F03623X/1, EP/J00961X/1]
- German Ministry for Education and Research [82DZL004A1]
- Telethon Foundation [TMLGCBX16TT]
- Engineering and Physical Sciences Research Council [EP/J00961X/1, EP/F03623X/1] Funding Source: researchfish
- EPSRC [EP/F03623X/1, EP/J00961X/1] Funding Source: UKRI
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 Ca2+-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.
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