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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man.

Chloride channels play important roles in the plasma membrane and in intracellular organelles. Mice deficient for the ubiquitously expressed ClC-7 Cl(-) channel show severe osteopetrosis and retinal degeneration. Although osteoclasts are present in normal numbers, they fail to resorb bone because they cannot acidify the extracellular resorption lacuna. ClC-7 resides in late endosomal and lysosomal compartments. In osteoclasts, it is highly expressed in the ruffled membrane, formed by the fusion of H(+)-ATPase-containing vesicles, that secretes protons into the lacuna. We also identified CLCN7 mutations in a patient with human infantile malignant osteopetrosis. We conclude that ClC-7 provides the chloride conductance required for an efficient proton pumping by the H(+)-ATPase of the osteoclast ruffled membrane.[1]

References

  1. Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man. Kornak, U., Kasper, D., Bösl, M.R., Kaiser, E., Schweizer, M., Schulz, A., Friedrich, W., Delling, G., Jentsch, T.J. Cell (2001) [Pubmed]
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