Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.

Ítems similars

• The ClC-5 knockout mouse model of Dent's disease has renal hypercalciuria and increased bone turnover.
  per: Silva, I, et al.
  Publicat: (2003)
• Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease.
  per: Devuyst, O, et al.
  Publicat: (1999)
• CLC-5 and KIF3B interact to facilitate CLC-5 plasma membrane expression, endocytosis, and microtubular transport: relevance to pathophysiology of Dent's disease.
  per: Reed, A, et al.
  Publicat: (2010)
• Comparative ontogeny, processing, and segmental distribution of the renal chloride channel, ClC-5.
  per: Jouret, F, et al.
  Publicat: (2004)
• Molecular pathology of renal chloride channels in Dent's disease and Bartter's syndrome.
  per: Thakker, R
  Publicat: (2000)