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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse KO Clcn5-/- model for Dents disease in kidney, bone and intestine

ABSTRACT: Mutations in ClC-5 cause Dent's disease, a disorder associated with low molecular weight proteinuria, hyperphosphaturia and kidney stones. ClC-5 is a Cl /H+-exchanger predominantly expressed in the kidney, where it facilitates the acidification of proximal tubular endosomes. The reduction in proximal tubular endocytosis resulting from a lack of ClC-5 raises the luminal concentration of filtered proteins and peptides like PTH.

We used gene expression profiling to identify possible signaling pathways that might be changed in ClC-5 KO kidneys, bones and intestines. Mouse model described in Piwon et al, ClC-5 Cl--channel disruption impairs endocytosis in a mouse model for Dent's disease, Nature 408, 369-373 (16 November 2000),doi: 10.1038/35042597

ORGANISM(S): Mus musculus

SUBMITTER: Gesa Rickheit

PROVIDER: E-MEXP-495 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Kidney-specific upregulation of vitamin D3 target genes in ClC-5 KO mice.

Maritzen T T Rickheit G G Schmitt A A Jentsch T J TJ

Kidney international 20060503 1

Mutations in ClC-5 cause Dent's disease, a disorder associated with low molecular weight proteinuria, hyperphosphaturia, and kidney stones. ClC-5 is a Cl(-)/H(+)-exchanger predominantly expressed in the kidney, where it facilitates the acidification of proximal tubular endosomes. The reduction in proximal tubular endocytosis resulting from a lack of ClC-5 raises the luminal concentration of filtered proteins and peptides like parathyroid hormone (PTH). The increase in PTH may explain the hyperph ...[more]

PMID: 16672909

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