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. Author manuscript; available in PMC: 2008 Jul 23.
Published in final edited form as: Exp Hematol. 2007 Jul;35(7):1026–1037. doi: 10.1016/j.exphem.2007.03.017

Figure 3. Deficiency of SFKs in hematopoietic stem and progenitor cells results in enhanced activation of Stat3, but normal differentiation.

Figure 3

Figure 3

(A) Lineage negative cells from wildtype and SFK−/− mice were stimulated with G-CSF for the indicated time points. Equal amount of protein was used to run a SDS-PAGE gel and probed with an anti-phospho-Stat3 antibody. Top panel shows the amount of phospho-Stat3 protein in each lane and the bottom panel shows equal protein in each lane as assessed by the presence of β-actin. (B) Wildtype and SFK−/− Lin− bone marrow cells were in vitro differentiated. After 48 and 72 hours, cells were harvested and stained with antibodies that recognize the cell surface marker Mac-1 and Gr-1. (C) Wildtype and SFK−/− mice were injected with 300 μg/kg/day of G-CSF for 4 days and bone marrow fluid was harvested. Equal amount of bone marrow fluid (200 μg) was used to run a 2-D SDS-PAGE gels. Shown is a representative 2-D gel that was fixed, stained with coomassie blue and destained with deionized water. Similar results were seen in three independent experiments. (D) Wildtype and SFK−/− mice were injected with 300 μg/kg/day of G-CSF for 4 days and plasma was harvested. Equal amount of plasma from wildtype and SFK−/− mice was used to measure MMP-9 levels by gelatin zymography as previously described. The top arrow indicates the level of Pro-MMP-9 and the bottom arrow indicates the amount of active MMP-9. Lanes 1 & 3 contain plasma from control wildtype and SFK−/− mice. Lanes 2 & 4 contain plasma from G-CSF treated wildtype and SFK−/− mice. Similar results were observed in three independent experiments.