Csf3r mutations in mice confer a strong clonal HSC advantage via activation of Stat5
J. Clin. Invest. Fulu Liu, et al. 118:946 doi:10.1172/JCI32704 [Go to this article.]

Figure 6
Stat5 deficiency abrogates the hyperproliferative response of the d715 G-CSFR in myeloid progenitors. E12–E15 fetal liver cells from wild-type or Stat5A^–/– × Stat5B^–/– (Stat5^–/–) mice were transduced with retrovirus expressing neomycin phosphotransferase alone (Neo) or this gene and either wild-type G-CSFR (WT GR) or d715 G-CSFR. Cells were cultured in 10 ng/ml of G-CSF and geneticin to select for transduced cells. Shown is the number of colonies (A) and average colony size (B) observed after 7–10 days. Similar results were observed in cultures stimulated with 1 ng/ml of G-CSF (data not shown). No colonies formed in the absence of G-CSF (data not shown). Data represent the mean ± SEM of 3 independent experiments.