Abstract
Alterations in Wnt/beta-catenin signaling have been linked to abnormal kidney development and tumorigenesis. To gain more insights into the effects of these alterations, we created mice carrying a conditional deletion of the Apc tumor suppressor gene specifically in the renal epithelium. As expected, the loss of Apc leads to increased levels of beta-catenin protein in renal epithelium. Most of these mice die shortly after birth, and multiple kidney cysts were found upon histological examination. Only rarely did these animals survive to adulthood. Analysis of these adults revealed severely cystic kidneys associated with the presence of renal adenomas. Our results confirm an important role for proper regulation of Wnt/beta-catenin signaling in renal development and provide evidence that dysregulation of the pathway can initiate tumorigenesis in the kidney.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenoma / mortality
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Adenoma / pathology
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Adenoma / physiopathology*
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Animals
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Cytoplasm / metabolism
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Cytoskeletal Proteins / metabolism
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Genes, APC / physiology*
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Integrases / genetics
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Intercellular Signaling Peptides and Proteins / metabolism
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Kidney Neoplasms / mortality
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Kidney Neoplasms / pathology
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Kidney Neoplasms / physiopathology*
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Kidney Tubules / pathology
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Kidney Tubules / physiopathology
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Mice
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Mice, Transgenic
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Polycystic Kidney Diseases / mortality
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Polycystic Kidney Diseases / pathology
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Polycystic Kidney Diseases / physiopathology*
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Trans-Activators / metabolism
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Urothelium / pathology
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Urothelium / physiopathology
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Wnt Proteins
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beta Catenin
Substances
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CTNNB1 protein, mouse
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Cytoskeletal Proteins
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Intercellular Signaling Peptides and Proteins
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Trans-Activators
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Wnt Proteins
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beta Catenin
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Cre recombinase
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Integrases