Cartron Pierre-François, Petit Elise, Bellot Grégory, Oliver Lisa, Vallette François M
Team 9 (Equipe labellisée Ligue Nationale contre le Cancer), Centre de Recherche en Cancérologie Nantes-Angers, UMR INSERM 892/CNRS UMR 6299, F-44007 Nantes, France; Université de Nantes, Faculté de Médecine, 9 Quai Moncousu, 44035 Nantes Cedex 01, France.
Team 9 (Equipe labellisée Ligue Nationale contre le Cancer), Centre de Recherche en Cancérologie Nantes-Angers, UMR INSERM 892/CNRS UMR 6299, F-44007 Nantes, France; Université de Nantes, Faculté de Médecine, 9 Quai Moncousu, 44035 Nantes Cedex 01, France; CHU de Nantes, 1 place Alexis-Ricordeau, 44093 Nantes Cedex 1, France.
Cell Signal. 2014 Sep;26(9):1928-34. doi: 10.1016/j.cellsig.2014.04.021. Epub 2014 May 2.
The proteins Bax and Bak are central in the execution phase of apoptosis; however, little is known about the partners involved in the control of this complex process. Here, we show that mitochondrial Bak is incorporated into a VDAC2/Mtx1/Mtx2 multi-protein complex in both resting and dying cells. VDAC2 is a porin that has previously been described as a partner of Bak while Mtx1 and Mtx2 are two proteins of the mitochondrial sorting and assembly machinery (SAM) that have been implicated in TNF-induced apoptosis. We show that, after the induction of apoptosis, Bak switches from its association with Mtx2 and VDAC2 to interact with Mtx1.
蛋白质Bax和Bak在细胞凋亡的执行阶段起着核心作用；然而，对于参与控制这一复杂过程的相关蛋白知之甚少。在此，我们发现，无论是在静止细胞还是濒死细胞中，线粒体Bak都能与一种包含VDAC2/Mtx1/Mtx2的多蛋白复合物相结合。VDAC2是一种孔蛋白，此前曾被描述为Bak的结合蛋白，而Mtx1和Mtx2是线粒体分选与组装机制（SAM）中的两种蛋白，它们与肿瘤坏死因子（TNF）诱导的细胞凋亡有关。我们发现，在诱导细胞凋亡后，Bak从与Mtx2和VDAC2的结合状态转变为与Mtx1相互作用。
