Article
ClC-5, the chloride channel mutated in Dent's disease, colocalizes with the proton pump in endocytotically active kidney cells.
Proceedings of the National Academy of Sciences of the United States of America - 7 Jul 1998
Günther W, Lüchow A, Cluzeaud F, Vandewalle A, Jentsch T J
Abstract excerpt
Loss-of-function mutations of the ClC-5 chloride channel lead to Dent's disease, a syndrome characterized by low molecular weight proteinuria, hypercalciuria, and kidney stones. We show that ClC-5 is expressed in renal proximal tubule cells, which normally endocytose proteins passing the glomerular filter. Expression is highest below the brush border in a region densely packed with endocytotic vesicles, where...
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