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Review
. 2007 Jun 15;13(12):3435-8.
doi: 10.1158/1078-0432.CCR-07-0810.

"No Turning Bax" in the combined battle against prostate cancer:

Ramji R Rajendran  1 , Gary D Kao
Affiliations
Review

"No Turning Bax" in the combined battle against prostate cancer:

Ramji R Rajendran et al. Clin Cancer Res. .
No abstract available

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Figures

Fig. 1
Fig. 1
The opposing roles of Bcl-2 and Bax in mediating apoptosis. Damage signals (e.g., resulting from hormonal ablation or cancer treatment, symbolized by the lightning bolt) result in the binding of BH3 domain – containing proteins to and the inactivation of Bcl-2.This in turns leads to the oligomerization of proapoptotic factors such as Bax, forming pores through which cytochrome c is released from the inner mitochondrial membrane into the cytosol. This then contributes to the formation of the apoptosome and the subsequent activation of caspase cascades, together bringing about apoptosis of the cell. In contrast, Bcl-2, when uninhibited, blocks Bax from permeabilizing the outer mitochondrial membrane, suppressing apoptosis.
See this image and copyright information in PMC

Comment on

References

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