Here, the authors used an inducible lentiviral vector to express Nurr1. They find that Foxm1 directly bound to the promoter region of the gene encoding the receptor Nurr1, inducing transcription, while forced expression of Nurr1 reversed the loss of quiescence observed in Foxm1-deficient cells in vivo. Thus, these studies reveal a previously unrecognized role for Foxm1 as a critical regulator of the quiescence and self-renewal of HSCs mediated at least in part by control of Nurr1 expression.
The authors tested a Doxycycline (Dox)-inducible “all-in-one” lentiviral vector (Lv.TII vectors) design which expresses a reverse transactivator protein (rtTA2S-M2) in human hematopoietic cells. Functionality of Dox-inducible hCDD expression was demonstrated by a more than 10-fold increase in cytosine arabinoside (Ara-C) resistance of Lv.TII.CDD transduced K562 cells. In addition, Lv.TII.CDD transduced CD34+ derived myeloid cells were protected from up to 300nM Ara-C.
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Here, the authors used an inducible lentiviral vector to express Nurr1. They find that Foxm1 directly bound to the promoter region of the gene encoding the receptor Nurr1, inducing transcription, while forced expression of Nurr1 reversed the loss of quiescence observed in Foxm1-deficient cells in vivo. Thus, these studies reveal a previously unrecognized role for Foxm1 as a critical regulator of the quiescence and self-renewal of HSCs mediated at least in part by control of Nurr1 expression.
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