Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man (Q28201425)

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D Kasper

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M R Bösl

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E Kaiser

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M Schweizer

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A Schulz

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W Friedrich

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G Delling

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T J Jentsch

Chloride channels of intracellular organelles.

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language of work or name

English

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publication date

26 January 2001

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published in

Cell

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volume

104

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page(s)

205-15

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issue

2

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cites work

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Cell-mediated extracellular acidification and bone resorption: evidence for a low pH in resorbing lacunae and localization of a 100-kD lysosomal membrane protein at the osteoclast ruffled border

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Axotomy results in delayed death and apoptosis of retinal ganglion cells in adult rats.

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Osteoclastic bone resorption by a polarized vacuolar proton pump

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ClC-6 and ClC-7 are two novel broadly expressed members of the CLC chloride channel family

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Biochemical markers of bone metabolism: an overview

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Defects in TCIRG1 subunit of the vacuolar proton pump are responsible for a subset of human autosomal recessive osteopetrosis

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The yeast CLC chloride channel functions in cation homeostasis

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The GEF1 gene of Saccharomyces cerevisiae encodes an integral membrane protein; mutations in which have effects on respiration and iron-limited growth.

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ClC-5, the chloride channel mutated in Dent's disease, colocalizes with the proton pump in endocytotically active kidney cells

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The CLC chloride channel family

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Mutations in the gene encoding B1 subunit of H+-ATPase cause renal tubular acidosis with sensorineural deafness

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Retinal atrophy in osteopetrosis

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Complete genomic structure of the CLCN6 and CLCN7 putative chloride channel genes(1).

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Mutations in the a3 subunit of the vacuolar H(+)-ATPase cause infantile malignant osteopetrosis

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Osteopetrosis and osteoporosis: two sides of the same coin

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Atp6i-deficient mice exhibit severe osteopetrosis due to loss of osteoclast-mediated extracellular acidification.

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A common molecular basis for three inherited kidney stone diseases

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Trafficking of Matrix Collagens Through Bone-Resorbing Osteoclasts

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Molecular cloning and expression of three isoforms of the 100-kDa a subunit of the mouse vacuolar proton-translocating ATPase.

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ClC-5 Cl- -channel disruption impairs endocytosis in a mouse model for Dent's disease.

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Impaired osteoclastic bone resorption leads to osteopetrosis in cathepsin-K-deficient mice

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Removal of osteoclast bone resorption products by transcytosis

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Characterization of the Osteoclast Ruffled Border Chloride Channel and Its Role in Bone Resorption

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Golgi localization and functionally important domains in the NH2 and COOH terminus of the yeast CLC putative chloride channel Gef1p

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Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III

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Carbonic anhydrase II deficiency identified as the primary defect in the autosomal recessive syndrome of osteopetrosis with renal tubular acidosis and cerebral calcification

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Disruption of ClC-3, a chloride channel expressed on synaptic vesicles, leads to a loss of the hippocampus

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Three subunit a isoforms of mouse vacuolar H(+)-ATPase. Preferential expression of the a3 isoform during osteoclast differentiation

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The bone marrow-derived stromal cell lines MC3T3-G2/PA6 and ST2 support osteoclast-like cell differentiation in cocultures with mouse spleen cells

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