Figure 1.
Figure 1. Conditional deletion of STAT3 in bone marrow. (A) Genomic tail DNA was analyzed by PCR using primers that detect wild-type (w), floxed (f), and deleted (Δ) STAT3 alleles or the TIE2cre transgene (+). (B) Bone marrow cells from wild-type (WT) or STAT3-deficient (KO) mice were stimulated with G-CSF (100 ng/mL) for 30 minutes or left untreated, as indicated. Immunoblots of whole cell lysates were probed with antibodies specific for phospho-STAT3, total STAT3, or total STAT5. (C) Peripheral blood samples from WT or KO mice were stained with Gr-1 and CD11b antibodies conjugated to FITC and PE, respectively, and analyzed by flow cytometry. The percentage of Gr-1+/CD11b+ cells in individual samples was plotted; bars indicate the mean for each group (P < .001 comparing WT with KO).

Conditional deletion of STAT3 in bone marrow. (A) Genomic tail DNA was analyzed by PCR using primers that detect wild-type (w), floxed (f), and deleted (Δ) STAT3 alleles or the TIE2cre transgene (+). (B) Bone marrow cells from wild-type (WT) or STAT3-deficient (KO) mice were stimulated with G-CSF (100 ng/mL) for 30 minutes or left untreated, as indicated. Immunoblots of whole cell lysates were probed with antibodies specific for phospho-STAT3, total STAT3, or total STAT5. (C) Peripheral blood samples from WT or KO mice were stained with Gr-1 and CD11b antibodies conjugated to FITC and PE, respectively, and analyzed by flow cytometry. The percentage of Gr-1+/CD11b+ cells in individual samples was plotted; bars indicate the mean for each group (P < .001 comparing WT with KO).

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