Figure 5
Figure 5. Survival of imatinib-treated v-Abl+ cells depends on the phosphorylation status of STAT5. (A) FACS profiles of cells infected with pMSCv-Stat5a-IRES-eGFP retrovirus before (left histogram) and after sort for GFP+ cells (middle histograms). Tyrosine phosphorylated STAT5 is shown in the right histograms. Right panel: Electrophoretic mobility shift assay of sorted GFP+ (S5ahigh) and GFP− (S5alow) cells for STAT5. Stat5null/null MEFs were used as negative control, and Ba/F3 stimulated with IL-3 were used as positive control. (B) Scheme of murine wild-type and mutant STAT5A variants. Mutants lacking the tyrosine phosphorylation (pY) site or having impaired DNA binding (DB) are indicated by either (+) or (−). (C) v-Abl+ cell lines expressing STAT5A, STAT5A mutants, or vector control along with GFP 24 hours after imatinib administration. The fold increase of GFP-expressing cells is shown. Error bars represent mean ± SD. ***P < .001 for a dosage of 1000nM imatinib (n ≥ 4/group).

Survival of imatinib-treated v-Abl+ cells depends on the phosphorylation status of STAT5. (A) FACS profiles of cells infected with pMSCv-Stat5a-IRES-eGFP retrovirus before (left histogram) and after sort for GFP+ cells (middle histograms). Tyrosine phosphorylated STAT5 is shown in the right histograms. Right panel: Electrophoretic mobility shift assay of sorted GFP+ (S5ahigh) and GFP (S5alow) cells for STAT5. Stat5null/null MEFs were used as negative control, and Ba/F3 stimulated with IL-3 were used as positive control. (B) Scheme of murine wild-type and mutant STAT5A variants. Mutants lacking the tyrosine phosphorylation (pY) site or having impaired DNA binding (DB) are indicated by either (+) or (−). (C) v-Abl+ cell lines expressing STAT5A, STAT5A mutants, or vector control along with GFP 24 hours after imatinib administration. The fold increase of GFP-expressing cells is shown. Error bars represent mean ± SD. ***P < .001 for a dosage of 1000nM imatinib (n ≥ 4/group).

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