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Restoring cancer's death sentence

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Presentation on theme: "Restoring cancer's death sentence"— Presentation transcript:

1 Restoring cancer's death sentence
Anthony Letai  Cancer Cell  Volume 10, Issue 5, Pages (November 2006) DOI: /j.ccr Copyright © 2006 Elsevier Inc. Terms and Conditions

2 Figure 1 Two models of BCL-2 inhibition of PCD
A: In Model A, activator BH3-only proteins are sequestered by BCL-2 at the mitochondrion, preserving survival (Aa) until treatment with ABT-737 displaces the activators, which then activate BAX or BAK, which oligomerize and induce MOMP (Ab). When abundant MCL-1 is present, activator displaced from BCL-2 by ABT-737 is bound by MCL-1, maintaining survival (Ac and Ad). B: In Model B, BCL-2 and MCL-1 keep activated BAX or BAK at bay (Ba). ABT-737 frees BAX or BAK from BCL-2, allowing oligomerization and MOMP (Bb). When abundant MCL-1 is present, BAX or BAK displaced from BCL-2 can be bound by MCL-1 to prevent PCD (Bc and Bd). Cancer Cell  , DOI: ( /j.ccr ) Copyright © 2006 Elsevier Inc. Terms and Conditions

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