title: Bcl-2 phosphorylation is not required for its effects on NFkappaB activity.
abstract: We have previously shown that in the aged CNS there is a free radical-dependent upregulation of Bcl-2 associated with perturbations of NFkappaB function. Both Bcl-2 and NFkappaB are key players in the cellular machinery devoted to cope with stress and regulate neuronal apoptosis. To study whether effects on NFkappaB are part of the Bcl-2 anti-apoptotic mechanism, we examined the effect of Bcl-2 on NFkappaB 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 NFkappaB-promoted transcription and that this effect is independent of Bcl-2 phosphorylation. We conclude that such Bcl-2 effect on NFkappaB activity is distinct from its anti-apoptotic action.
authors.affiliation: Department of Anatomy and Neurosciences, University of Texas Medical Branch, Galveston, TX 77555, USA.
authors.forename: Cynthia A
authors.initials: CA
authors.lastname: Massaad
authors.forename: Giulio
authors.initials: G
authors.lastname: Taglialatela
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D015153:Blotting, Western / Q000379:methods; D002460:Cell Line; D002478:Cells, Cultured; D005786:Gene Expression Regulation; D017930:Genes, Reporter / Q000502:physiology; D005822:Genetic Vectors / Q000378:metabolism; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D016716:PC12 Cells; D010766:Phosphorylation; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D051381:Rats; D013997:Time Factors; D014162:Transfection; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
chemical_list: D016328:NF-kappa B; D019253:Proto-Oncogene Proteins c-bcl-2; D014409:Tumor Necrosis Factor-alpha; D000469:Alkaline Phosphatase