Bcl-2 phosphorylation is not required for its effects on NFκB activity

We have previously shown that in the aged CNS there is a free radical-dependent upregulation of Bcl-2 associated with perturbations of NFκB function. Both Bcl-2 and NFκB are key players in the cellular machinery devoted to cope with stress and regulate neuronal apoptosis. To study whether effects on NFκB are part of the Bcl-2 anti-apoptotic mechanism, we examined the effect of Bcl-2 on NFκB transcriptional activity in PC12 cells and determined the role thereby of Bcl-2 phosphorylation (required for the anti-apoptotic function of Bcl-2). Our results indicate that over-expression of Bcl-2 significantly decreases NFκB-promoted transcription and that this effect is independent of Bcl-2 phosphorylation. We conclude that such Bcl-2 effect on NFκB activity is distinct from its anti-apoptotic action.