Fig. 2.
Fig. 2. Overexpression of Bcl-2 or Bcl-xL inhibited Apo-2L–induced apoptosis of HL-60 cells (A). / Following treatment with 100 ng/mL of Apo-2L, the percentage of apoptotic cells was determined by Annexin V staining and flow cytometry (A). Western blot analyses of Bcl-2 and Bcl-xL levels demonstrating overexpression of Bcl-2 and Bcl-xLin HL-60/Bcl-2 and HL-60/ Bcl-xL cells, respectively. Levels of β-actin served as the loading control (B). Cotreatment with the relatively specific caspase-8 inhibitor (z-IETD-fmk, 50 μmol/L) or caspase-9 inhibitor (z-LEHD-fmk, 100 μmol/L) inhibited Apo-2L–induced apoptosis (C).

Overexpression of Bcl-2 or Bcl-xL inhibited Apo-2L–induced apoptosis of HL-60 cells (A).

Following treatment with 100 ng/mL of Apo-2L, the percentage of apoptotic cells was determined by Annexin V staining and flow cytometry (A). Western blot analyses of Bcl-2 and Bcl-xL levels demonstrating overexpression of Bcl-2 and Bcl-xLin HL-60/Bcl-2 and HL-60/ Bcl-xL cells, respectively. Levels of β-actin served as the loading control (B). Cotreatment with the relatively specific caspase-8 inhibitor (z-IETD-fmk, 50 μmol/L) or caspase-9 inhibitor (z-LEHD-fmk, 100 μmol/L) inhibited Apo-2L–induced apoptosis (C).

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