Figure 5
Figure 5. Treatment of cells with PFT-α rescues the erythroid phenotype of ribosomal gene shRNAs. (A) After infection of CD34+ cells with either a control (luciferase) gene or ribosomal gene shRNAs, cells were treated with different concentrations of PFT-α, an inhibitor of p53 function. After 72 hours, expression of p21 mRNA, relative to β-actin, was analyzed by quantitative RT-PCR. (B) The ratio of erythroid to myeloid lineage cells was also analyzed by flow cytometry using antibodies against surface markers GlyA (erythroid) and CD11b (myeloid) after 8 days in culture. Results of PFT-α experiments are representative of 2 independent experiments performed in triplicate (mean ± SEM). *P < .05. **P < .01.

Treatment of cells with PFT-α rescues the erythroid phenotype of ribosomal gene shRNAs. (A) After infection of CD34+ cells with either a control (luciferase) gene or ribosomal gene shRNAs, cells were treated with different concentrations of PFT-α, an inhibitor of p53 function. After 72 hours, expression of p21 mRNA, relative to β-actin, was analyzed by quantitative RT-PCR. (B) The ratio of erythroid to myeloid lineage cells was also analyzed by flow cytometry using antibodies against surface markers GlyA (erythroid) and CD11b (myeloid) after 8 days in culture. Results of PFT-α experiments are representative of 2 independent experiments performed in triplicate (mean ± SEM). *P < .05. **P < .01.

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