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Review
, 108 (7), 965-9

The Survivin Saga Goes in Vivo

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Review

The Survivin Saga Goes in Vivo

J C Reed. J Clin Invest.

Figures

Figure 1
Figure 1
Models for Survivin function. Several models are proposed that might explain how Survivin directly or indirectly inhibits caspases. Survivin might directly bind and inhibit caspase, analogous to IAPs, such as XIAP (top). Survivin might sequester SMAC, thus protecting IAPs from this inhibitory protein (middle). Finally, Survivin might somehow enhance the function of IAPs, having a function opposite to SMAC (bottom).
Figure 2
Figure 2
Two routes to apoptosis. In the “intrinsic” cell death pathway, various upstream stimuli, such as activation of p53, induce expression or activation of proapoptotic Bcl-2 family proteins (e.g., Bax, Puma, Noxa) that converge on mitochondria and induce cytochrome c release. In the cytosol, cytochrome c binds Apaf1, which activates caspase-9. In the “extrinsic” pathway, TNF-family receptors trigger caspase-8 activation. Active caspase-8 and caspase-9 cleave and activate caspase-3 and possibly other downstream effector caspases. Caspase-8 can also cleave and activate Bid, resulting in mitochondrial release of cytochrome c. Once activated, downstream caspases can also damage mitochondria, representing a potential amplification mechanism. The putative point of Survivin intervention at caspase-9 is shown. Cdc2 may be required for apoptosis suppression by Survivin. Expression of Cdc2 can be repressed by p53 in G2-phase. DD, death domain; DED, death effector domain.

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