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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Bax, but not Bcl-x_L, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations
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Bax, but not Bcl-x_L, decreases the lifetime of planar phospholipid bilayer membranes at subnanomolar concentrations

机译：Bax而不是Bcl-x_L会降低亚纳摩尔浓度的平面磷脂双层膜的寿命

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摘要

Release of proteins through the outer mito-chondrial membrane can be a critical step in apoptosis, and the localization of apoptosis-regulating Bcl-2 family members there suggests they control this process. We used planar phospholipid membranes to test the effect of full-length Bax and Bcl-x_L synthesized in vitro and native Bax purified from bovine thymocytes. Instead of forming pores with reproducible conductance levels expected for ionic channels, Bax, but not Bcl-x_L, created arbitrary and continuously variable changes in membrane permeability and decreased the stability of the membrane, regardless of whether the source of the protein was synthetic or native. This breakdown of the membrane permeability barrier and destabilization of the bilayer was quantified by using membrane lifetime measurements. Bax decreased membrane lifetime in a voltage- and concentration-dependent manner. Bcl-x_L did not protect against Bax-induced membrane destabilization, supporting the idea that these two proteins function independently. Corresponding to a physical theory for lipidic pore formation, Bax potently diminished the linear tension of the membrane (i.e., the energy required to form the edge of a new pore). We suggest that Bax acts directly by destabilizing the lipid bilayer structure of the outer mitochondrial membrane, promoting the formation of a pore—the apoptotic pore—large enough to allow mitochondrial proteins such as cytochrome c to be released into the cytosol. Bax could then enter and perme-abilize the inner mitochondrial membrane through the same hole.
机译：蛋白质通过线粒体外膜的释放可能是细胞凋亡的关键步骤，而细胞凋亡调节性Bcl-2家族成员的定位表明它们可以控制这一过程。我们使用平面磷脂膜来测试全长Bax和Bcl-x_L在体外合成以及从牛胸腺细胞纯化的天然Bax的作用。 Bax而非形成离子通道所期望的可重现电导率水平的孔，而不是Bcl-x_L创造了膜渗透率的任意连续变化，并降低了膜的稳定性，无论蛋白质的来源是合成的还是天然的。膜渗透性屏障的破坏和双层的失稳通过使用膜寿命测量来量化。 Bax以依赖电压和浓度的方式降低了膜的寿命。 Bcl-x_L不能防止Bax引起的膜不稳定，支持这两种蛋白独立起作用的观点。与脂质孔形成的物理理论相对应，Bax有效地降低了膜的线性张力（即，形成新孔的边缘所需的能量）。我们建议Bax通过使线粒体外膜的脂质双层结构不稳定来直接起作用，从而促进形成一个孔（凋亡孔），该孔足够大以允许线粒体蛋白（例如细胞色素c）释放到细胞质中。然后Bax可以通过同一孔进入并渗透线粒体内膜。

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