Herrmann J L, Bruckheimer E, McDonnell T J
University of Texas M.D. Anderson Cancer Center, Department of Molecular Pathology, Houston, TX 77030, USA.
Biochem Soc Trans. 1996 Nov;24(4):1059-65. doi: 10.1042/bst0241059.
The mechanism by which Bcl-2 can insulate cells against multiple diverse apoptotic signals is largely undefined. How is it possible that Bcl-2, which possesses no known catalytic function, can protect against multiple cell-death signals? A proposal to address this question postulates that Bcl-2 functions at convergence points common to most cell-death signal-transduction pathways. This review attempts to integrate observations regarding cell-death signalling in an effort to define points of convergence. The ceramide/ SAPK/JNK and NF kappa B pathways, in particular, were emphasized. Potential points at which Bcl-2 may function frequently involve the transmembrane trafficking of molecules implicated in the mediation of apoptosis. The selectivity of this process and the effector proteins with which Bcl-2 associated remain to be elucidated.
Bcl-2能够使细胞免受多种不同凋亡信号影响的机制在很大程度上尚不清楚。没有已知催化功能的Bcl-2如何能够抵御多种细胞死亡信号呢?针对这个问题的一种假设认为,Bcl-2在大多数细胞死亡信号转导途径共有的汇聚点起作用。本综述试图整合有关细胞死亡信号传导的观察结果,以确定汇聚点。特别强调了神经酰胺/SAPK/JNK和核因子κB途径。Bcl-2可能起作用的潜在点常常涉及参与凋亡介导的分子的跨膜运输。这个过程的选择性以及与Bcl-2相关的效应蛋白仍有待阐明。