| License: Creative Commons Attribution 4.0 PDF - Published Version (10MB) |
- URN to cite this document:
- urn:nbn:de:bvb:355-epub-447181
- DOI to cite this document:
- 10.5283/epub.44718
This publication is part of the DEAL contract with Springer.
Abstract
Polycystic kidney disease (PKD) leads to continuous decline of renal function by growth of renal cysts. Enhanced proliferation and transepithelial chloride secretion through cystic fibrosis transmembrane conductance regulator (CFTR) and Ca2+-activated TMEM16A Cl- channels is thought to cause an increase in cyst volume. Recent work shows the pro-proliferative role of the Ca2+ activated Cl- channel ...
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