Journal
GENES & DEVELOPMENT
Volume 24, Issue 15, Pages 1614-1619Publisher
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.1942810
Keywords
miR-451; microRNA-451; erythroid differentiation; 14-3-3 zeta; ywhaz; antagomir
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Funding
- NIH [HL089966, HL09530601A1]
- Robert A. Welch Foundation
- American Heart Association-Jon Holden DeHaan Foundation
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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. 14-3-3 zeta, an intracellular regulator of cytokine signaling that is repressed by miR-451, is up-regulated in miR-451(-/-) erythroblasts, and inhibition of 14-3-3 zeta rescues their differentiation defect. These findings reveal an essential role of 14-3-3 zeta as a mediator of the proerythroid differentiation actions of miR-451, and highlight the therapeutic potential of miR-451 inhibitors.
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