Leber Brian, Andrews David W
F1000 Biol Rep. 2010 Dec 17;2:88. doi: 10.3410/B2-88.
While there is a clear connection between apoptosis and autophagy, the mechanisms that regulate the interaction have been difficult to identify. The initial clue to the link was the observation that Bcl-2 was located at the endoplasmic reticulum (ER), where it could prevent some forms of apoptosis and also bind to the autophagy regulatory protein Beclin-1. However, both of these enigmatic observations have been united with the discovery of the nutrient-deprivation autophagy factor-1 (NAF-1) protein. As an ER-localized protein that enhances the interaction of Bcl-2 and Beclin-1 and that also binds to the pro-apoptotic protein Bik, NAF-1 is perfectly placed to be a central regulator of the switch between autophagy and apoptosis.
虽然细胞凋亡与自噬之间存在明确的联系，但调节两者相互作用的机制却难以确定。两者联系的最初线索是观察到Bcl-2定位于内质网（ER），在那里它可以阻止某些形式的细胞凋亡，并且还能与自噬调节蛋白Beclin-1结合。然而，这两个神秘的观察结果随着营养剥夺自噬因子-1（NAF-1）蛋白的发现而联系在一起。作为一种内质网定位蛋白，NAF-1可增强Bcl-2与Beclin-1的相互作用，并且还能与促凋亡蛋白Bik结合，因此它完全有条件成为自噬与细胞凋亡转换的核心调节因子。
