Dent's disease. (1/9)

ATP induces conformational changes in the carboxyl-terminal region of ClC-5. (2/9)

Mouse model for Lowe syndrome/Dent Disease 2 renal tubulopathy. (3/9)

Chloride channel (Clc)-5 is necessary for exocytic trafficking of Na+/H+ exchanger 3 (NHE3). (4/9)

Suppression of intestinal calcium entry channel TRPV6 by OCRL, a lipid phosphatase associated with Lowe syndrome and Dent disease. (5/9)

Inositol 5-phosphatases: insights from the Lowe syndrome protein OCRL. (6/9)

An atypical Dent's disease phenotype caused by co-inheritance of mutations at CLCN5 and OCRL genes. (7/9)

Conformational defects underlie proteasomal degradation of Dent's disease-causing mutants of ClC-5. (8/9)

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