Figure 6.
Figure 6. s-SLP-65–mediated apoptosis is diminished after BCR stimulation.(A) BCR-induced apoptosis mediated by SLP-65 and s-SLP-65. SLP-65–deficient cells (top row) or transfectants expressing either full-length or s-SLP-65 (middle and bottom rows, respectively) were left untreated or stimulated through their BCR for 24 hours (left and right panels, respectively). Following staining of the cells with 7-AAD and annexin V–PE, early and late apoptotic cells were identified by flow cytometry. (B) Statistical evaluation and influence of MAPK inhibition on SLP-65–regulated cell death. Apoptotic rates of resting and BCR-stimulated cells were calculated for 3 independent clones analyzed at least 2 times as described in panel A and for cells pretreated prior to BCR activation with 2.5 μM p38-i (SB202190, ▨) or 5 μM JNK-i (SP600125, ▦) to inhibit p38 and JNK, respectively. Error bars indicate SD of 9 independent experiments.

s-SLP-65–mediated apoptosis is diminished after BCR stimulation.(A) BCR-induced apoptosis mediated by SLP-65 and s-SLP-65. SLP-65–deficient cells (top row) or transfectants expressing either full-length or s-SLP-65 (middle and bottom rows, respectively) were left untreated or stimulated through their BCR for 24 hours (left and right panels, respectively). Following staining of the cells with 7-AAD and annexin V–PE, early and late apoptotic cells were identified by flow cytometry. (B) Statistical evaluation and influence of MAPK inhibition on SLP-65–regulated cell death. Apoptotic rates of resting and BCR-stimulated cells were calculated for 3 independent clones analyzed at least 2 times as described in panel A and for cells pretreated prior to BCR activation with 2.5 μM p38-i (SB202190, ▨) or 5 μM JNK-i (SP600125, ▦) to inhibit p38 and JNK, respectively. Error bars indicate SD of 9 independent experiments.

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