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

First Author  Patrick DM Year  2010
Journal  Genes Dev Volume  24
Issue  15 Pages  1614-9
PubMed ID  20679397 Mgi Jnum  J:163251
Mgi Id  MGI:4821499 Doi  10.1101/gad.1942810
Citation  Patrick DM, et al. (2010) Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta. Genes Dev 24(15):1614-9
abstractText  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.
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