Reference : Nicotinamide phosphoribosyl transferase/pre-B cell colony-enhancing factor/visfatin i...
Scientific journals : Article
Life sciences : Veterinary medicine & animal health
Nicotinamide phosphoribosyl transferase/pre-B cell colony-enhancing factor/visfatin is required for lymphocyte development and cellular resistance to genotoxic stress.
Rongvaux, Anthony [> > > >]
Galli, Mara [> > > >]
Denanglaire, Sebastien [> > > >]
Van Gool, Frederic [> > > >]
Dreze, Pierre L [> > > >]
Szpirer, Claude [> > > >]
Bureau, Fabrice mailto [Université de Liège - ULiège > Département de sciences fonctionnelles > GIGA-R : Biochimie et biologie moléculaire >]
Andris, Fabienne [> > > >]
Leo, Oberdan [> > > >]
Journal of Immunology
American Association of Immunologists
Yes (verified by ORBi)
[en] Animals ; Cell Death/genetics/immunology ; Cell Differentiation/drug effects/genetics/immunology ; Cell Line ; Cell Survival/genetics/immunology ; Cytokines/biosynthesis/deficiency/genetics/physiology ; Gene Deletion ; Humans ; Immunity, Cellular/drug effects/genetics
[en] Nicotinamide phosphoribosyl transferase (Nampt)/pre-B cell colony-enhancing factor (PBEF)/visfatin is a protein displaying multiple functional properties. Originally described as a cytokine-like protein able to regulate B cell development, apoptosis, and glucose metabolism, this protein also plays an important role in NAD biosynthesis. To gain insight into its physiological role, we have generated a mouse strain expressing a conditional Nampt allele. Lack of Nampt expression strongly affects development of both T and B lymphocytes. Analysis of hemizygous cells and in vitro cell lines expressing distinct levels of Nampt illustrates the critical role of this protein in regulating intracellular NAD levels. Consequently, a clear relationship was found between intracellular Nampt levels and cell death in response to the genotoxic agent MNNG (N-methyl-N'-nitro-N-nitrosoguanidine), confirming that this enzyme represents a key regulator of cell sensitivity to NAD-consuming stress secondary to poly(ADP-ribose) polymerases overactivation. By using mutant forms of this protein and a well-characterized pharmacological inhibitor (FK866), we unequivocally demonstrate that the ability of the Nampt to regulate cell viability during genotoxic stress requires its enzymatic activity. Collectively, these data demonstrate that Nampt participates in cellular resistance to genotoxic/oxidative stress, and it may confer to cells of the immune system the ability to survive during stressful situations such as inflammation.
Researchers ; Professionals ; Students

File(s) associated to this reference

Fulltext file(s):

Restricted access
RongvauxA_JImmunol_.pdfNo commentaryPublisher postprint654.12 kBRequest copy

Bookmark and Share SFX Query

All documents in ORBi are protected by a user license.