西亚试剂：Defective erythroid differentiation in miR-451 mutant mice

Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3ζ
David M. Patrick, Cheng C. Zhang, Ye Tao, Huiyu Yao, Xiaoxia Qi, Robert J. Schwartz, Lily Jun-Shen Huang, and Eric N. Olson

1Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;
2Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;
3Department of Developmental Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;
4Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, Texas 77030, USA;
5Department of Cell Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA;
6Texas Heart Institute, Texas Medical Center, Houston, Texas 77030, USA;
7Department of Biology and Biochemistry, The University of Houston, Houston, Texas 77004, USA

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. 14-3-3ζ, an intracellular regulator of cytokine signaling that is repressed by miR-451, is up-regulated in miR-451?/? erythroblasts, and inhibition of 14-3-3ζ rescues their differentiation defect. These findings reveal an essential role of 14-3-3ζ as a mediator of the proerythroid differentiation actions of miR-451, and highlight the therapeutic potential of miR-451 inhibitors.

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