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

Cynthia A. Massaad, Giulio Taglialatela

Research output: Contribution to journalArticle

3 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1167-1170
Number of pages4
JournalNeuroReport
Volume14
Issue number8
DOIs
StatePublished - Jun 11 2003

Keywords

  • Bcl-2
  • NFκB
  • Oxidative stress
  • Phosphorylation

ASJC Scopus subject areas

  • Neuroscience(all)

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