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T. Wang et al.
chimeras. Surprisingly, only a few Nupr1-/-Mdm2+/- HSC were present in the HSC pool of the recipients, while the Nupr1-/- HSC dominantly occupied the HSC pool (Figure 6D, E). Overall, the reversal of p53 expression offset the competitive advantage of Nupr1-/- HSC.
Deletion of Nupr1 in adulthood in the Nupr1fl/fl Mx1-cre model also promoted hematopoietic stem cell engraftment
In the Nupr1fl/fl Vav-Cre model, the Nupr1 locus was delet- ed at an embryonic stage. To exclude the possibility that the
A
effects of loss of Nupr1 observed in adulthood is a conse- quence of an effect coming from the embryo, Nupr1fl/fl mice were crossed with Mx1-Cre mice to generate induced Nupr1 knockout mice at an adult stage in the presence of polyinosinic-polycytidylic acid (pIpC). The deletion of the Nupr1 gene in the Nupr1fl/flMx1-cre mice was verified by PCR in HSC (Online Supplementary Figure S1D, E). Consistent with the observation of loss of Nupr1 in the Nupr1fl/fl Vav-Cre model, significantly more Nupr1fl/flMx1-cre HSC entered the G1-S-S2 and M phases (median value: 26.35%) than their counterparts from littermate control
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Figure 6. Figure continued on following page.
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