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. Author manuscript; available in PMC: 2013 Mar 19.
Published in final edited form as: Nat Rev Drug Discov. 2008 Jan 19;8(2):153–171. doi: 10.1038/nrd2780

Figure 6. Physiology of selected voltage-gated (ClC)-type chloride channels.

Figure 6

a | ClC-1 in skeletal muscle stabilizes membrane potential. ClC-1 loss-of-function mutations causes myotonia. b | ClC-Kb in the basolateral membrane of kidney distal tubular cells facilitates transepithelial sodium chloride absorption, through coordinated activity with the apical bumetanide-sensitive Na+/K+/2Cl− cotransporter, apical potassium channel (to recycle potassium in the tubule lumen) and basolateral Na+/K+-ATPase. c | ClC-5 in kidney proximal tubule epithelial cells facilitates endocytosis and endosomal acidification. ClC-5 loss-of function mutations cause proteinuria and kidney stones (Dent’s disease). Organellar ClCs such as ClC-5 and ClC-7 function as electrogenic Cl−/H+ exchangers. d | ClC-7 chloride transport in bone osteoclasts facilitates net secretion of HCl into the lacuna for bone demineralization. ClC-7 loss-of-function mutations cause osteopetrosis. ACh, acetylcholine.