Boya P, Kroemer G
3D Lab (Development, Differentiation & Degeneration), Department of Cellular and Molecular Physiopathology, Centro de Investigaciones Biológicas, CSIC, Ramiro de Maetzu 9, Madrid, Spain.
Oncogene. 2009 May 28;28(21):2125-7. doi: 10.1038/onc.2009.83. Epub 2009 Apr 27.
Beclin 1 has been recently shown to possess a Bcl-2 homology-3 (BH3) domain that mediates its interaction with antiapoptotic multidomain proteins. Unlike other BH3-only proteins, Beclin 1 fails to stimulate apoptosis when it is overexpressed. In this issue of Oncogene, Ciechomska et al. report the intriguing finding that Bcl-2, as it interacts with Beclin 1, does not lose its anti-apoptotic potential. This finding may have far-reaching implications for the comprehension of the cross-talk between apoptosis and autophagy.
最近研究表明，Beclin 1拥有一个Bcl-2同源结构域3（BH3），该结构域介导其与抗凋亡多结构域蛋白的相互作用。与其他仅含BH3结构域的蛋白不同，Beclin 1过表达时并不能刺激细胞凋亡。在本期《癌基因》杂志中，Ciechomska等人报道了一个有趣的发现：Bcl-2在与Beclin 1相互作用时，并未丧失其抗凋亡潜能。这一发现可能对理解细胞凋亡与自噬之间的相互作用有着深远的意义。
