2. Holinger JBC 274, 13298-304, 1999

3. Stapled alpha-helix of BCL-2 domains (SAHB) Walensky Science 305, 1466-70, 2004

6. Proposed mechanism of bcl-2 pore formation

14. Gottlob et al., Genes Dev 2001

17. Akt inhibits Bax/Bak activation ( Majewski, Mol Cell Biol 2004 ) Bid displaces mitochondrial hexokinase ( ibid ) Conditions leading to loss of mitochondrial hexokinase induce apoptosis even in Bax/Bak -/- cells, and are rescued by Akt, but not Bcl-2 ( Majewski, Mol Cell 2004 )

20. Copyright ©2005 American Society for Clinical Investigation Levine, B. et al. J. Clin. Invest. 2005;115:2679-2688 The autophagy pathway and its role in cellular adaptation to nutrient deprivation

21. Copyright ©2005 American Society for Clinical Investigation Levine, B. et al. J. Clin. Invest. 2005;115:2679-2688 The molecular mechanisms of autophagy

22. Copyright ©2005 American Society for Clinical Investigation Levine, B. et al. J. Clin. Invest. 2005;115:2679-2688 Ultrastructural examples of apoptotic and autophagic cell death

23. Lum et al., 2005

25. Shimizu et al., Nat Cell Biol 2004

26. Autophagy is a response to nutrient stress to maintain adequate internal levels of nutrients(self-cannabilization). Role in cell death is best revealed if apoptosis is disabled (bax/bak-/-, caspase inhibitors, Bcl-xL++). In nutrient-poor conditions (or equivalent effects on mTOR signaling), autophagy maintains survival. In nutrient-rich conditions, autophagy promotes cell death in response to other types of stress.