Cellular and subcellular immunolocalization of ClC-5 channel in mouse kidney: colocalization with H+-ATPase.

No abstract is available for this paper.

• Publication year

  1999

• Venue

  AJP - Renal Physiology

• Publication date

  1999-12-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1152/ajprenal.1999.277.6.F957PMID 29591633
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

• The swelling-activated chloride channel ClC-2, the chloride channel ClC-3, and ClC-5, a chloride channel mutated in kidney stone disease, are expressed in distinct subpopulations of renal epithelial cells.

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• Idiopathic low molecular weight proteinuria associated with hypercalciuric nephrocalcinosis in Japanese children is due to mutations of the renal chloride channel (CLCN5).

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• Identification of a New Outwardly Rectifying Cl Channel That Belongs to a Subfamily of the ClC Cl Channels (*)

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• A common molecular basis for three inherited kidney stone diseases

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• Identification of distinct subpopulations of intercalated cells in the mouse collecting duct.

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• Physiology and biochemistry of the kidney vacuolar H+-ATPase.

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• Cloning and Functional Expression of Rat CLC-5, a Chloride Channel Related to Kidney Disease (*)

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• Stable and functional expression of the CIC-3 chloride channel in somatic cell lines.

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• Transport from late endosomes to lysosomes, but not sorting of integral membrane proteins in endosomes, depends on the vacuolar proton pump

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• Endosomal alkalinization reduces Jmax and Km of albumin receptor-mediated endocytosis in OK cells.

  1995cited by this paper
• Cloning and characterization of CLCN5, the human kidney chloride channel gene implicated in Dent disease (an X-linked hereditary nephrolithiasis).

  1995cited by this paper
• Properties of voltage‐gated chloride channels of the ClC gene family.

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• Characterization of a human and murine gene (CLCN3) sharing similarities to voltage-gated chloride channels and to a yeast integral membrane protein.

  1995cited by this paper
• Hypercalciuria and nephrocalcinosis in patients with idiopathic low-molecular-weight proteinuria in Japan: is the disease identical to Dent's disease in United Kingdom?

  1995cited by this paper
• Dent's disease; a familial proximal renal tubular syndrome with low-molecular-weight proteinuria, hypercalciuria, nephrocalcinosis, metabolic bone disease, progressive renal failure and a marked male predominance.

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• Vacuolar ATPase activity is required for endosomal carrier vesicle formation.

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• Mapping the gene causing X-linked recessive nephrolithiasis to Xp11.22 by linkage studies.

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• Dent's disease, a renal Fanconi syndrome with nephrocalcinosis and kidney stones, is associated with a microdeletion involving DXS255 and maps to Xp11.22.

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• Cloning and expression of apical membrane water channel of rat kidney collecting tubule

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• Immunologic evidence that vacuolar H+ ATPases with heterogeneous forms of Mr = 31,000 subunit have different membrane distributions in mammalian kidney.

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• From protein uptake to Dent disease: an overview of the CLCN5 gene.

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• A novel CLCN5 pathogenic mutation supports Dent disease with normal endosomal acidification

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• ClC-5: Physiological role and biophysical mechanisms.

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• Mutations associated with Dent's disease affect gating and voltage dependence of the human anion/proton exchanger ClC-5

  2015influential citation
• Molecular mechanisms and regulation of urinary acidification.

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• Aquaporins with anion/monocarboxylate permeability: mechanisms, relevance for pathogen–host interactions

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• Chloride in vesicular trafficking and function.

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• Functional coupling of chloride–proton exchanger ClC-5 to gastric H+,K+-ATPase

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  2012cites this paper
• Cell biology and physiology of CLC chloride channels and transporters.

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• The interaction between megalin and ClC-5 is scaffolded by the Na⁺-H⁺ exchanger regulatory factor 2 (NHERF2) in proximal tubule cells.

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• Dent’s disease: clinical features and molecular basis

  2011cites this paper
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• ClC-5 mutations associated with Dent’s disease: a major role of the dimer interface

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