Figure 5
Figure 5. Signaling defects in Ptpn11Δ/Δ LSK and LK cells. Lin− BM cells from control (n = 4) and Ptpn11Δ/Δ (n = 4) mice were purified by FACS and starved for 1 hour in serum-free media, before they were either left untreated or stimulated with SCF (50 ng/mL) or TPO (50 ng/mL) for the indicated times. Cells were fixed, permeabilized, and stained with anti–c-kit, anti-Sca1, and anti-pErk (A-B) or pAkt (C-D). Levels of phospho-specific antigens in the LSK and LK population were determined by flow cytometry. The percentages of pErk+ or pAkt+ cells from 4 experiments are shown as mean ± SEM. *P < .05, Student t test.

Signaling defects in Ptpn11Δ/Δ LSK and LK cells. Lin BM cells from control (n = 4) and Ptpn11Δ/Δ (n = 4) mice were purified by FACS and starved for 1 hour in serum-free media, before they were either left untreated or stimulated with SCF (50 ng/mL) or TPO (50 ng/mL) for the indicated times. Cells were fixed, permeabilized, and stained with anti–c-kit, anti-Sca1, and anti-pErk (A-B) or pAkt (C-D). Levels of phospho-specific antigens in the LSK and LK population were determined by flow cytometry. The percentages of pErk+ or pAkt+ cells from 4 experiments are shown as mean ± SEM. *P < .05, Student t test.

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