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The PI3K pathway balances self-renewal and differentiation of nephron progenitor cells through ?-catenin signaling.


ABSTRACT: Nephron progenitor cells differentiate to form nephrons during embryonic kidney development. In contrast, self-renewal maintains progenitor numbers and premature depletion leads to impaired kidney function. Here we analyze the PI3K pathway as a point of convergence for the multiple pathways that are known to control self-renewal in the kidney. We demonstrate that a reduction in PI3K signaling triggers premature differentiation of the progenitors and activates a differentiation program that precedes the mesenchymal-to-epithelial transition through ectopic activation of the ?-catenin pathway. Therefore, the combined output of PI3K and other pathways fine-tunes the balance between self-renewal and differentiation in nephron progenitors.

SUBMITTER: Lindstrom NO 

PROVIDER: S-EPMC4400645 | biostudies-literature | 2015 Apr

REPOSITORIES: biostudies-literature

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The PI3K pathway balances self-renewal and differentiation of nephron progenitor cells through β-catenin signaling.

Lindström Nils Olof NO   Carragher Neil Oliver NO   Hohenstein Peter P  

Stem cell reports 20150305 4


Nephron progenitor cells differentiate to form nephrons during embryonic kidney development. In contrast, self-renewal maintains progenitor numbers and premature depletion leads to impaired kidney function. Here we analyze the PI3K pathway as a point of convergence for the multiple pathways that are known to control self-renewal in the kidney. We demonstrate that a reduction in PI3K signaling triggers premature differentiation of the progenitors and activates a differentiation program that prece  ...[more]

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