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Copyright ©The Author(s) 2017.
World J Nephrol. Jan 6, 2017; 6(1): 14-20
Published online Jan 6, 2017. doi: 10.5527/wjn.v6.i1.14
Figure 1
Figure 1 Effects of CLC-5 inactivation on endosomal acidification and endocytosis. A: In CLC-5 knockout mice, both endosomal acidification and endocytosis are impaired, resulting in a Dent’s disease-like phenotype; B: E211A, an artificial mutation of the gating glutamate of CLC-5, converts its function from a 2Cl-/H+ antiporter into a pure Cl- conductance. E211A knock-in mice exhibit defective endocytosis and manifestations similar to those observed in Dent’s disease manifestations but retain normal endosomal acidification.
Figure 2
Figure 2 Potential roles of CLC-5 in endosomes. A: In this model, Cl- accumulation by CLC-5 is critical for normal endocytosis; B: In contrast, 2Cl-/H+ exchange mode of CLC-5 activates V-ATPase which is required for maximal endosomal acidification.