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...
主要な著者: | Wang, S, Devuyst, O, Courtoy, P, Wang, X, Wang, H, Wang, Y, Thakker, R, Guggino, S, Guggino, W |
---|---|
フォーマット: | Journal article |
言語: | English |
出版事項: |
2000
|
類似資料
-
The ClC-5 knockout mouse model of Dent's disease has renal hypercalciuria and increased bone turnover.
著者:: Silva, I, 等
出版事項: (2003) -
Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease.
著者:: Devuyst, O, 等
出版事項: (1999) -
CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's disease.
著者:: Reed, A, 等
出版事項: (2010) -
Comparative ontogeny, processing, and segmental distribution of the renal chloride channel, ClC-5.
著者:: Jouret, F, 等
出版事項: (2004) -
Molecular pathology of renal chloride channels in Dent's disease and Bartter's syndrome.
著者:: Thakker, R
出版事項: (2000)