| Experiment Id | E-MEXP-495 | Name | Transcription profiling by array of mouse Clcn5 knockout in kidney, bone and intestine |
| Experiment Type | transcription profiling by array | Study Type | WT vs. Mutant |
| Source | ArrayExpress | Curation Date | 2018-03-02 |
| description | 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 |
