ClC-5: a chloride channel with multiple roles in renal tubular albumin uptake.

No abstract is available for this paper.

• Publication year

  2006

• Venue

  International Journal of Biochemistry and Cell Biology

• Publication date

  Unknown publication date

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1016/J.BIOCEL.2005.09.009PMID 16226913
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

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• Impaired acidification in early endosomes of ClC-5 deficient proximal tubule.

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• Chloride/proton antiporter activity of mammalian CLC proteins ClC-4 and ClC-5

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• Voltage-dependent electrogenic chloride/proton exchange by endosomal CLC proteins

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• Renal tubule albumin transport.

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• ClC-5: role in endocytosis in the proximal tubule.

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• PKC-alpha-mediated remodeling of the actin cytoskeleton is involved in constitutive albumin uptake by proximal tubule cells.

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• Physiological functions of CLC Cl- channels gleaned from human genetic disease and mouse models.

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• Identification of a novel splice site mutation of CLCN5 gene and characterization of a new alternative 5′ UTR end of ClC-5 mRNA in human renal tissue and leukocytes

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• Reduced renal ClC-5 Cl- channel expression in spontaneously hypertensive rats with microalbuminuria.

  2004cited by this paper
• Functional and structural conservation of CBS domains from CLC chloride channels

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• Relative Contribution of Nedd4 and Nedd4-2 to ENaC Regulation in Epithelia Determined by RNA Interference*

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• Why is proteinuria an ominous biomarker of progressive kidney disease?

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• Nedd4-2 Functionally Interacts with ClC-5

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• MOLECULAR CHANGES IN PROXIMAL TUBULE FUNCTION IN DIABETES MELLITUS

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• NHE3 Na+/H+ exchanger supports proximal tubular protein reabsorption in vivo.

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• Loss of chloride channel ClC-5 impairs endocytosis by defective trafficking of megalin and cubilin in kidney proximal tubules

  2003cited by this paper
• Altered polarity and expression of H+-ATPase without ultrastructural changes in kidneys of Dent's disease patients.

  2003cited by this paper
• Cofilin Interacts with ClC-5 and Regulates Albumin Uptake in Proximal Tubule Cell Lines*

  2003cited by this paper
• Renal handling of albumin: a critical review of basic concepts and perspective.

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• CLC chloride channels: correlating structure with function.

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• X-ray structure of a ClC chloride channel at 3.0 Å reveals the molecular basis of anion selectivity

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• Pre- and Postnatal Lung Development, Maturation, and Plasticity ClC-5: ontogeny of an alternative chloride channel in respiratory epithelia

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• Inhibition of Na+‐H+ exchanger‐3 interferes with apical receptor‐mediated endocytosis via vesicle fusion

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• Expression and regulation of ClC-5 chloride channels: effects of antisense and oxidants.

  2001cited by this paper
• An Internalization Signal in ClC-5, an Endosomal Cl−Channel Mutated in Dent's Disease*

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• Megalin and cubilin: synergistic endocytic receptors in renal proximal tubule.

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• Glomerular protein sieving and implications for renal failure in Fanconi syndrome.

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

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• Physiology of renal sodium transport.

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• Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.

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• Isolation and characterization of the human CLC-5 chloride channel gene promoter.

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• Molecular Links between Endocytosis and the Actin Cytoskeleton

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• Molecular Cloning and Characterization of an Intracellular Chloride Channel in the Proximal Tubule Cell Line, LLC-PK1*

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• Inhibition of Na+‐H+ exchange impairs receptor‐mediated albumin endocytosis in renal proximal tubule‐derived epithelial cells from opossum

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• All Three WW Domains of Murine Nedd4 Are Involved in the Regulation of Epithelial Sodium Channels by Intracellular Na+ *

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• Intra-renal and subcellular distribution of the human chloride channel, CLC-5, reveals a pathophysiological basis for Dent's disease.

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• Nedd4 mediates control of an epithelial Na+ channel in salivary duct cells by cytosolic Na+.

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• A common molecular basis for three inherited kidney stone diseases

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

  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
• Sorting and recycling efficiency of apical insulin binding sites during endocytosis in proximal tubule cells.

  1993cited by this paper
• Dent's disease, a renal Fanconi syndrome with nephrocalcinosis and kidney stones, is associated with a microdeletion involving DXS255 and maps to Xp11.22.

  1993cited by this paper
• Endocytosis in proximal tubule cells involves a two-phase membrane-recycling pathway.

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• Sodium-hydrogen exchange and glucose transport in renal microvillus membrane vesicles from rats with diabetes mellitus.

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• Emerging Perspectives on the Rare Tubulopathy Dent Disease: Is Glomerular Damage a Direct Consequence of ClC-5 Dysfunction?

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• Role of ion channels in the mechanism of proteinuria (Review)

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• Diversity of functional alterations of the ClC‐5 exchanger in the region of the proton glutamate in patients with Dent disease 1

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

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• A rare case of nephrotic syndrome associated with Dent’s disease: a case report

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

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• Protein Uptake at Glomerular Level: Possible Involvement of an Endocytic Machinery in Cell Culture and in Patients with Lupus Nephritis

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• Hereditary causes of kidney stones and chronic kidney disease

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• endocytic machinery in the renal proximal tubule with lower expression of critical components of the apical Progression of microalbuminuria in SHR is associated

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• Formation of the urine proteome of healthy humans

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• Characterization of Disease-causing Mutations in the Chloride-Proton Antiporter ClC-5

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