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...
المؤلفون الرئيسيون: | Wang, S, Devuyst, O, Courtoy, P, Wang, X, Wang, H, Wang, Y, Thakker, R, Guggino, S, Guggino, W |
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التنسيق: | Journal article |
اللغة: | English |
منشور في: |
2000
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مواد مشابهة
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The ClC-5 knockout mouse model of Dent's disease has renal hypercalciuria and increased bone turnover.
حسب: Silva, I, وآخرون
منشور في: (2003) -
Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease.
حسب: Devuyst, O, وآخرون
منشور في: (1999) -
CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's disease.
حسب: Reed, A, وآخرون
منشور في: (2010) -
Comparative ontogeny, processing, and segmental distribution of the renal chloride channel, ClC-5.
حسب: Jouret, F, وآخرون
منشور في: (2004) -
Molecular pathology of renal chloride channels in Dent's disease and Bartter's syndrome.
حسب: Thakker, R
منشور في: (2000)