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Genes Dev. 2010 Aug 1;24(15):1614-9. doi: 10.1101/gad.1942810.

Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta.

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1
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA.

Abstract

Erythrocyte formation occurs throughout life in response to cytokine signaling. We show that microRNA-451 (miR-451) regulates erythropoiesis in vivo. Mice lacking miR-451 display a reduction in hematrocrit, an erythroid differentiation defect, and ineffective erythropoiesis in response to oxidative stress. 14-3-3zeta, an intracellular regulator of cytokine signaling that is repressed by miR-451, is up-regulated in miR-451(-/-) erythroblasts, and inhibition of 14-3-3zeta rescues their differentiation defect. These findings reveal an essential role of 14-3-3zeta as a mediator of the proerythroid differentiation actions of miR-451, and highlight the therapeutic potential of miR-451 inhibitors.

PMID:
20679397
PMCID:
PMC2912559
DOI:
10.1101/gad.1942810
[Indexed for MEDLINE]
Free PMC Article

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