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Article

Receptor-mediated endocytosis and endosomal acidification is impaired in proximal tubule epithelial cells of Dent disease patients.

Proceedings of the National Academy of Sciences of the United States of America - 23 Apr 2013

Gorvin Caroline M, Wilmer Martijn J, Piret Sian E, Harding Brian, van den Heuvel Lambertus P, Wrong Oliver, Jat Parmjit S, Lippiat Jonathan D, Levtchenko Elena N, Thakker Rajesh V

Abstract excerpt

Receptor-mediated endocytosis, involving megalin and cubilin, mediates renal proximal-tubular reabsorption and is decreased in Dent disease because of mutations of the chloride/proton antiporter, chloride channel-5 (CLC-5), resulting in low-molecular-weight proteinuria, hypercalciuria, nephrolithiasis, and renal failure. To facilitate studies of receptor-mediated endocytosis and the role of CLC-5, we established...

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Share to Chloride Channels
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Kidney Tubules, Proximal

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Source

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Identifiers

PMID: 23572577
DOI: 10.1073/pnas.1302063110
PMCID: PMC3637698

Genes

CLC
VAMP2

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Receptor-mediated endocytosis and endosomal acidification is impaired in proximal tubule epithelial cells of Dent disease patients.PMID 23572577Read ↗

TMEM9 and SEC22B interact with ClC-5 to shape renal proximal tubule function and Dent’s Disease type I pathogenesisSemantic proximity Read ↗

Novel Dent disease 1 cellular models reveal biological processes underlying ClC-5 loss-of-function.Semantic proximity Read ↗

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

ClC transporters: discoveries and challenges in defining the mechanisms underlying function and regulation of ClC-5.Semantic proximity Read ↗

A pure chloride channel mutant of CLC-5 causes Dent's disease via insufficient V-ATPase activation.Semantic proximity Read ↗

A novel CLCN5 pathogenic mutation supports Dent disease with normal endosomal acidification.Semantic proximity Read ↗

The chloride channel ClC-4 contributes to endosomal acidification and trafficking.Semantic proximity Read ↗

Kidney Tubular Ablation of Ocrl/Inpp5b Phenocopies Lowe Syndrome Tubulopathy.Semantic proximity Read ↗

Functional characterization of a novel missense CLCN5 mutation causing alterations in proximal tubular endocytic machinery in Dent's disease.Semantic proximity Read ↗

Dent's disease: chloride-proton exchange controls proximal tubule endocytosis.Semantic proximity Read ↗

Global gene-expression analysis reveals the molecular processes underlying ClC-5 loss-of-function in novel Dent Disease 1 cellular modelsSemantic proximity Read ↗

A Focus on the Proximal Tubule Dysfunction in Dent Disease Type 1.Semantic proximity Read ↗

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