Fig. 5.
Fig. 5. BAY 36-1677 induces apoptosis in leukemic lymphoblasts. / KOPN57bi cells were exposed for 7 days to BAY 36-1677 (25 ng/mL) and then labeled with annexin V FITC and propidium iodide (PI; top panels). Flow cytometric density plots show binding of annexin V in BAY 36-1677–treated cells, indicating exposure of phosphatidylserine residues on the cell membrane (early stages of apoptosis), and PI labeling, indicating membrane permeabilization (late-stage cell death). Bottom panels illustrate DNA content analysis and staining with dUTP FITC, which labels cells with fragmented DNA. BAY 36-1677 caused DNA fragmentation and hypodiploidy, both characteristic of apoptosis.

BAY 36-1677 induces apoptosis in leukemic lymphoblasts.

KOPN57bi cells were exposed for 7 days to BAY 36-1677 (25 ng/mL) and then labeled with annexin V FITC and propidium iodide (PI; top panels). Flow cytometric density plots show binding of annexin V in BAY 36-1677–treated cells, indicating exposure of phosphatidylserine residues on the cell membrane (early stages of apoptosis), and PI labeling, indicating membrane permeabilization (late-stage cell death). Bottom panels illustrate DNA content analysis and staining with dUTP FITC, which labels cells with fragmented DNA. BAY 36-1677 caused DNA fragmentation and hypodiploidy, both characteristic of apoptosis.

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