Abstract
Analyzing the regulatory mechanisms that control self-renewal and differentiation of hematopoietic stem cells (HSCs) is important to understand the pathophysiology of certain hematopoietic diseases and to succeed in expanding multipotent HSCs for therapy ex vivo. In a gene trap mouse model, the functional impairment of the transcriptional regulator Far Upstream Element Binding Protein 1 (FUBP1) led to embryonic lethality at day E15.5. Homozygous Fubp1-/- embryos showed largely reduced numbers of long-term repopulating (LT-) HSCs in the fetal liver, and lower engraftment of Fubp1-/- fetal liver cells was observed in competitive transplantation experiments.
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