Reference : Accumulation of the pro-apoptotic factor Bak is controlled by antagonist factor Mcl-1...
Scientific journals : Article
Human health sciences : Oncology
http://hdl.handle.net/2268/84908
Accumulation of the pro-apoptotic factor Bak is controlled by antagonist factor Mcl-1 availability
English
Minet, Emmanuel [ > > ]
Cosse, Jean-Philippe mailto [Université de Liège - ULg > > GIGA-R : Epigénétique Cellulaire et Moléculaire >]
Demazy, Catherine [ > > ]
Raes, Martine [ > > ]
Michiels, Carine [ > > ]
2006
Apoptosis : An International Journal on Programmed Cell Death
Kluwer Academic Publishers
11
1039-1047
Yes (verified by ORBi)
International
1360-8185
1573-675X
Boston
MA
[en] Bak ; Mcl-1
[en] Apoptosis has become recognized as a crucial mechanism
involved in a wide range of physiological and pathological
processes. Following an initial pro-apoptotic signal,
controlling phases allow the cell to reinforce or downgrade
signals leading to the irrevocable entry into apoptosis. Bak
(Bcl-2-antagonist killer) is a mitochondrial pore-forming
pro-apoptotic effector inhibited through titration by the antiapoptotic
protein Mcl-1 (Myeloid cell leukemia-1). Viruses
have taken advantage of proteasome-dependent degradation
of Bak as a mechanism to prevent apoptosis in infected
cells. It is not clear however whether regulation of Bak protein
level is involved in other physiological processes. In this
report, we show that Mcl-1 level is paralleled by Bak while
a Mcl-1 non-interacting mutant of Bak does not accumulate
in cells. This mechanism is proteasome independent.
Following serum withdrawal, Bak accumulation becomes
independent of Mcl-1 level and cells are sensitized to proapoptotic
stimuli. Based on these results, we propose that
regulation of Mcl-1-Bak steochiometry is a control mechanism
used as a checkpoint to prevent or allow entry into
apoptosis.
Unité de Recherche en Biologie Cellulaire
Facultés Universitaires Notre-Dame de La Paix
Researchers
http://hdl.handle.net/2268/84908
10.1007/s10495-006-6650-5

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