Figure 5.
Figure 5. Cell cycle analysis of CKR516-STAT1β– and CKR516-STAT1α–transfected cells treated or not treated with fludarabine. EGFP-positive and -negative cells were sorted by fluorescence-activated cell sorting (FACS) as for Figure 4A, after treatment of the cells with 0.6 μg/mL doxycycline for 24 hours. (A) Difference in proliferation rates of the EGFP-positive and -negative purified cells from CKR516-STAT1β–transfected cells. The 2 cell populations were grown in the presence (▪) or absence (⋄) of doxycycline over 4 days and were counted each day. The experiment was repeated twice. (B) Resistance to fludarabine-induced inhibition of cell proliferation in CKR516-STAT1β–transfected cells. EGFP-positive and -negative cell populations were purified by FACS after doxycycline treatment and were further treated or not treated with 15 μM fludarabine for 16 hours. The cell cycle was analyzed by flow cytometry after BrdU incorporation. The percentage of cells in the S phase is indicated within each diagram. (C) Absence of resistance to fludarabine-induced inhibition of cell proliferation in CKR516-STAT1α–transfected cells. As for panel B, the EGFP-positive and -negative cell populations purified by FACS were further treated with 15 μM fludarabine or left untreated. The percentage of cells in the S phase is indicated within each diagram. Results are representative of at least 2 independent experiments.

Cell cycle analysis of CKR516-STAT1β– and CKR516-STAT1α–transfected cells treated or not treated with fludarabine. EGFP-positive and -negative cells were sorted by fluorescence-activated cell sorting (FACS) as for Figure 4A, after treatment of the cells with 0.6 μg/mL doxycycline for 24 hours. (A) Difference in proliferation rates of the EGFP-positive and -negative purified cells from CKR516-STAT1β–transfected cells. The 2 cell populations were grown in the presence (▪) or absence (⋄) of doxycycline over 4 days and were counted each day. The experiment was repeated twice. (B) Resistance to fludarabine-induced inhibition of cell proliferation in CKR516-STAT1β–transfected cells. EGFP-positive and -negative cell populations were purified by FACS after doxycycline treatment and were further treated or not treated with 15 μM fludarabine for 16 hours. The cell cycle was analyzed by flow cytometry after BrdU incorporation. The percentage of cells in the S phase is indicated within each diagram. (C) Absence of resistance to fludarabine-induced inhibition of cell proliferation in CKR516-STAT1α–transfected cells. As for panel B, the EGFP-positive and -negative cell populations purified by FACS were further treated with 15 μM fludarabine or left untreated. The percentage of cells in the S phase is indicated within each diagram. Results are representative of at least 2 independent experiments.

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