Table 1.
Gene/molecule | Effects |
Bcl-2 subfamily (Ced9 in Caenorhabditis elegans) | |
Bcl-2 | Promotes survival |
Bcl-xl | Promotes survival |
Bcl-w | Promotes survival |
Bcl-xs | Promotes death |
Bax family | |
Bax | Promotes death |
Bak | Promotes death |
Bok | Promotes death |
BH3 subfamily | |
Bad | Promotes death |
Bik | Promotes death |
Bid | Promotes death |
Blk | Promotes death |
HRK | Promotes death |
BimL | Promotes death |
Egl (C elegans) | Promotes death |
Caspases 1–13* (Ced3 in C elegans) | These interleukin 1β converting enzyme (ICE) like cysteine proteinases form a central part of the apoptotic cascade |
Apaf-1 (Ced4 in C elegans) | These adaptor molecules link caspase (Ced3) activation and Bcl-2 (Ced9) expression. Their functions in promoting death or survival remain to be defined |
p53 family of tumour supressor genes | p53 is necessary for apoptosis induced by agents that cause DNA damage. Growth arrest occurs by activation of p21. p53 can also affect the expression of bcl-2 and bax directly. p21/WAF1 inhibits cyclin dependent kinases and prevents progression through the cell cycle |
Nitric oxide | This molecule prevents apoptosis by altering bcl-2 expression and by nitrosylation of caspases |
Cytochrome c | This molecule induces apoptosis via caspase activation |
This table summarises the major families of regulatory genes that are activated when a cell undergoes apoptosis. The list is by no means exhaustive but gives representative family members.
The products of the bcl-2 gene subfamily are mitochondrial proteins that can exist as homodimers or heterodimers made up of different pairings. Their functions are still unclear but changes in the ratio of their expression has profound effects on cell survival.
*Inhibitors of ICE have also been described recently.