ORBi: Minet Emmanuel - Accumulation of the pro-apoptotic factor Bak is controlled by antagonist factor Mcl-1 availability

Reference : Accumulation of the pro-apoptotic factor Bak is controlled by antagonist factor Mcl-1 av...


	Document type :	Scientific journals : Article
	Discipline(s) :	Human health sciences : Oncology
	To cite this reference:	http://hdl.handle.net/2268/84908

Title :	Accumulation of the pro-apoptotic factor Bak is controlled by antagonist factor Mcl-1 availability
Language :	English
Author, co-author :	Minet, Emmanuel [ > > ]
	Cosse, Jean-Philippe [Université de Liège - ULg > > GIGA-R : Epigénétique Cellulaire et Moléculaire >]
	Demazy, Catherine [ > > ]
	Raes, Martine [ > > ]
	Michiels, Carine [ > > ]
Publication date :	2006
Journal title :	Apoptosis : An International Journal on Programmed Cell Death
Publisher :	Kluwer Academic Publishers
Volume :	11
Pages :	1039-1047
Audience :	International
ISSN :	1360-8185
e-ISSN :	1573-675X
City :	Boston
Country :	MA
Keywords :	[en] Bak ; Mcl-1
Abstract :	[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.
Research units :	Unité de Recherche en Biologie Cellulaire
Funders :	Facultés Universitaires Notre-Dame de La Paix
Target :	Researchers
Permalink :	http://hdl.handle.net/2268/84908
DOI :	10.1007/s10495-006-6650-5

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