Figure 4.
Figure 4. Working model for the regulatory circuit involving miR-223, C/EBPα, and NFI-A in neutrophil differentiation. Experimental results47 are consistent with the idea that NFI-A and C/EBPα compete for binding to partially overlapping DNA sequences in the miR-223 gene promoter, and as long as NFI-A is present, this miR gene is inactive. Cells committed to granulocytic differentiation express C/EBPα, which activates miR-223 expression, resulting in repression of its NFI-A mRNA target. Thus, miR-223 appears to participate in a simple regulatory circuit of TFs that control granulopoiesis and may help stabilize the neutrophil phenotype induced by C/EBPα. Reprinted from Fazi et al47 with permission.

Working model for the regulatory circuit involving miR-223, C/EBPα, and NFI-A in neutrophil differentiation. Experimental results47  are consistent with the idea that NFI-A and C/EBPα compete for binding to partially overlapping DNA sequences in the miR-223 gene promoter, and as long as NFI-A is present, this miR gene is inactive. Cells committed to granulocytic differentiation express C/EBPα, which activates miR-223 expression, resulting in repression of its NFI-A mRNA target. Thus, miR-223 appears to participate in a simple regulatory circuit of TFs that control granulopoiesis and may help stabilize the neutrophil phenotype induced by C/EBPα. Reprinted from Fazi et al47  with permission.

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