Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.
Nephrolithiasis (kidney stones) affects 5-10% of adults and is most commonly associated with hypercalciuria, which may be due to monogenic renal tubular disorders. One such hypercalciuric disorder is Dent's disease, which is characterized by renal proximal tubular defects that include low molec...
Main Authors: | Wang, S, Devuyst, O, Courtoy, P, Wang, X, Wang, H, Wang, Y, Thakker, R, Guggino, S, Guggino, W |
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פורמט: | Journal article |
שפה: | English |
יצא לאור: |
2000
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פריטים דומים
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The ClC-5 knockout mouse model of Dent's disease has renal hypercalciuria and increased bone turnover.
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Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease.
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CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's disease.
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Comparative ontogeny, processing, and segmental distribution of the renal chloride channel, ClC-5.
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Molecular pathology of renal chloride channels in Dent's disease and Bartter's syndrome.
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