The ability of Bcl10 to protect from BCR-induced growth arrest and apoptosis is dependent on NF-κB. WEHI-231 cells (3 × 105/mL) expressing Bcl10-ER were treated with different combinations of β-estradiol (E2, 1 μM), anti-IgM (10 μg/mL), and NF-κB inhibitory peptide (NBD, 50 μM). NBD is a cell-permeable peptide containing sequences from the IκB kinase (IKK) γ subunit and from HIV-1 tat. This peptide inhibits NF-κB activation by blocking assembly of a functional IKK complex. The number of viable cells was determined in triplicate 48 hours after treatment, as in Figure 1. A control peptide containing a sequence from the L-plastin protein did not exhibit any effect on Bcl10-mediated protection against BCR-induced growth inhibition or apoptosis (not shown). ▪ indicates Bcl10-ER; ▦, Nonexpressors.
