期刊
BLOOD
卷 107, 期 11, 页码 4308-4316出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2005-06-2216
关键词
-
类别
资金
- NCI NIH HHS [N01-CO-12400] Funding Source: Medline
C/EBP alpha is an essential transcription factor required for myeloid differentiation. While C/EBP alpha can act as a cell fate switch to promote granulocyte differentiation in bipotential granulocyte-macrophage progenitors (GMPs), its role in regulating cell fate decisions in more primitive progenitors is not known. We found increased numbers of erythroid progenitors and erythroid cells in C/EBP alpha(-/-) fetal liver (FL). Also, enforced expression of C/EBP alpha in hematopoietic stem cells resulted in a loss of erythroid progenitors and an increase in myeloid cells by inhibition of erythroid development and inducing myeloid differentiation. Conditional expression of C/EBPa in murine erythroleukemia (MEL) cells induced myeloid-specific genes, while inhibiting erythroid-specific gene expression including erythropoietin receptor (EpoR), which suggests a novel mechanism to determine hematopoietic cell fate. Thus, C/EBP alpha functions in hematopoietic cell fate decisions by the dual actions of inhibiting erythroid and inducing myeloid gene expression in multipotential progenitors.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据