Figure 4.
Figure 4. Bcl-xL stabilizes the Δψm and abrogates the BCR coupling to the postmitochondrial activation of cathepsin B in WEHI-231 immature B cells. (A) WEHI-231-Neo (□) and WEHI-231-Bcl-xL (▪) immature B cells were treated with anti-Ig (10 μg/mL) or arachidonic acid (100 μM) for 24 hours, and mitochondrial potential was assessed using the dye DiOC6. The data are represented as the change in mean fluorescence intensity (MFI) of DiOC6 staining following stimulation to demonstrate the extent of depolarization. WEHI-231-Neo (B) or -Bcl-xL (C) immature B cells were stimulated for 24 hours with anti-Ig (10 μg/mL), and cell lysates were prepared. Cathepsin B activity as evidenced by cleavage of the cathepsin B substrate, zRR-pNA (z-Arg-Arg-pNA; Calbiochem), was then assayed as described in “Materials and methods.” Data are representative of at least 3 independent experiments. Error bars indicate means ± SDs; n = 3.

Bcl-xLstabilizes the Δψmand abrogates the BCR coupling to the postmitochondrial activation of cathepsin B in WEHI-231 immature B cells. (A) WEHI-231-Neo (□) and WEHI-231-Bcl-xL (▪) immature B cells were treated with anti-Ig (10 μg/mL) or arachidonic acid (100 μM) for 24 hours, and mitochondrial potential was assessed using the dye DiOC6. The data are represented as the change in mean fluorescence intensity (MFI) of DiOC6 staining following stimulation to demonstrate the extent of depolarization. WEHI-231-Neo (B) or -Bcl-xL (C) immature B cells were stimulated for 24 hours with anti-Ig (10 μg/mL), and cell lysates were prepared. Cathepsin B activity as evidenced by cleavage of the cathepsin B substrate, zRR-pNA (z-Arg-Arg-pNA; Calbiochem), was then assayed as described in “Materials and methods.” Data are representative of at least 3 independent experiments. Error bars indicate means ± SDs; n = 3.

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