Figure 1.
Figure 1. G-CSF–induced HPC mobilization in G-CSFR mutant mice. (A) Schematic of targeted G-CSFR mutations. Cytoplasmic tyrosines (Y) and the conserved box 1 and box 2 motifs are indicated. In the d715F mutant, the sole remaining tyrosine (Y704) of the G-CSFR has been mutated to phenylalanine (F). (B) Tissue distribution of HPCs following G-CSF treatment. Wild-type (WT) and G-CSFR mutant mice (n = 4, each) were treated with G-CSF (250 μg/kg/d) for 5 days and the number of CFU-Cs in blood, spleen, and bone marrow quantified 4 hours after the final dose of G-CSF. Data represent the mean ± SD. *P < .05 compared with G-CSF–treated WT mice.

G-CSF–induced HPC mobilization in G-CSFR mutant mice. (A) Schematic of targeted G-CSFR mutations. Cytoplasmic tyrosines (Y) and the conserved box 1 and box 2 motifs are indicated. In the d715F mutant, the sole remaining tyrosine (Y704) of the G-CSFR has been mutated to phenylalanine (F). (B) Tissue distribution of HPCs following G-CSF treatment. Wild-type (WT) and G-CSFR mutant mice (n = 4, each) were treated with G-CSF (250 μg/kg/d) for 5 days and the number of CFU-Cs in blood, spleen, and bone marrow quantified 4 hours after the final dose of G-CSF. Data represent the mean ± SD. *P < .05 compared with G-CSF–treated WT mice.

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