Fig. 4.
Fig. 4. Inhibition of PI3 kinase leads to a G1 cell cycle arrest in Ba/F3-TEL/PDGFβR cells. / Ba/F3-TEL/PDGFβR cells were grown to subconfluence and replated at 2 × 105 cells/mL in the absence (striped bars) or presence of 0.5 ng/mL IL-3 (black bars). (A) Cells were left untreated (control), treated with DMSO, or indicated inhibitor for 24 hours. Cells were harvested by centrifugation, stained with propidium iodide, and analyzed for DNA content. Percentage of cells with 2N DNA content was estimated by using the Modfit software. Data are the average of 2 experiments with Ba/F3-TEL/PDGFβR cells; similar results were obtained with 32D-TEL/PDGFβR cells (n = 2). (B) To determine the time course of cell cycle arrest, Ba/F3-TEL/PDGFβR cells were left untreated (closed squares), treated with DMSO alone (closed diamonds), or treated with LY294002 at 25 μM (closed circles) for the indicated time periods. Data are representative of 4 experiments with both Ba/F3-TEL/PDGFβR and 32D-TEL/PDGFβR cells.

Inhibition of PI3 kinase leads to a G1 cell cycle arrest in Ba/F3-TEL/PDGFβR cells.

Ba/F3-TEL/PDGFβR cells were grown to subconfluence and replated at 2 × 105 cells/mL in the absence (striped bars) or presence of 0.5 ng/mL IL-3 (black bars). (A) Cells were left untreated (control), treated with DMSO, or indicated inhibitor for 24 hours. Cells were harvested by centrifugation, stained with propidium iodide, and analyzed for DNA content. Percentage of cells with 2N DNA content was estimated by using the Modfit software. Data are the average of 2 experiments with Ba/F3-TEL/PDGFβR cells; similar results were obtained with 32D-TEL/PDGFβR cells (n = 2). (B) To determine the time course of cell cycle arrest, Ba/F3-TEL/PDGFβR cells were left untreated (closed squares), treated with DMSO alone (closed diamonds), or treated with LY294002 at 25 μM (closed circles) for the indicated time periods. Data are representative of 4 experiments with both Ba/F3-TEL/PDGFβR and 32D-TEL/PDGFβR cells.

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