title: WNT/β-catenin signaling in polycystic kidney disease.
abstract: Cystic kidney diseases have been linked to defective WNT signal transduction. Perturbations of cystic disease genes cause activation of canonical WNT/β-catenin/TCF/Lef1 signaling in model organisms and cultured cells. Inappropriate levels of WNT/β-catenin signaling cause renal cyst formation in mice. These observations have prompted the idea that an activation of WNT/β-catenin signaling may constitute a common causative event in cyst formation. Now this view is challenged by key genetic mouse models of cystic kidney disease that do not display WNT/β-catenin activity in cyst-lining epithelia.
authors: Max Delbrück Center for Molecular Medicine, Berlin, Germany.
authors: Anne
authors: A
authors: Wuebken
authors: Kai M
authors: KM
authors: Schmidt-Ott
mesh_terms: D000818:Animals; D003560:Cysts / Q000209:etiology*; D016891:Polycystic Kidney, Autosomal Dominant / Q000378:metabolism*; D051820:TCF Transcription Factors / Q000235:genetics*; D051176:beta Catenin / Q000378:metabolism*
chemical_list: C495267:CTNNB1 protein, mouse; D051820:TCF Transcription Factors; D051176:beta Catenin