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ClC-5, the chloride channel mutated in Dent’s disease, colocalizes with the proton pump in endocytotically active kidney cells

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...

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Auteurs principaux: Günther, Willy, Lüchow, Anke, Cluzeaud, Françoise, Vandewalle, Alain, Jentsch, Thomas J.
Format: Artigo
Langue:Inglês
Publié: The National Academy of Sciences 1998
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Accès en ligne:https://ncbi.nlm.nih.gov/pmc/articles/PMC20931/
https://ncbi.nlm.nih.gov/pubmed/9653142
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