Figure 1.
Figure 1. PIM1-deficiency or -inhibition enhances HSC mobilization in combination with AMD3100-treatment. (A) Statistical analysis of CXCR4 surface expression on Pim1-/- or WT LSK cells after AMD3100-treatment for 24h. PIM1-deficiency reverts the increased CXCR4 surface expression after AMD3100-treatment. (B) Time course of total LSK cells per ml PB of AMD3100-treated mice. Pim1-/- mice show significantly higher LSK counts. (C) Statistical analysis of total LSK cells per ml of LGB321+AMD3100 treated mice compared to AMD3100-only treated WT animals. PIM-inhibition significantly increases mobilization efficiency of AMD3100.

PIM1-deficiency or -inhibition enhances HSC mobilization in combination with AMD3100-treatment. (A) Statistical analysis of CXCR4 surface expression on Pim1-/- or WT LSK cells after AMD3100-treatment for 24h. PIM1-deficiency reverts the increased CXCR4 surface expression after AMD3100-treatment. (B) Time course of total LSK cells per ml PB of AMD3100-treated mice. Pim1-/- mice show significantly higher LSK counts. (C) Statistical analysis of total LSK cells per ml of LGB321+AMD3100 treated mice compared to AMD3100-only treated WT animals. PIM-inhibition significantly increases mobilization efficiency of AMD3100.

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