It is a well-established concept in the field of apoptosis that relative amounts of pro- and anti-survival Bcl-2 family of proteins determine whether the cell will undergo cell death; if more<unk>  is present, then pores are non-permeable to pro-apoptotic molecules and the cell survives. However, if Bax and Bak become activated, and<unk>  is sequestered away by gatekeeper BH3-only factors (e.g. Bim) causing a pore to form, cytochrome c is released leading to initiation of caspase cascade and apoptotic events. While the exact signaling pathway of<unk>  is still not known, it is believed that<unk>  differs highly from Bcl-2 in their mechanism of inducing apoptosis.<unk>  is about ten times more functional than Bcl-2 when induced by the chemotherapy drug, Doxorubicin and can specifically bind to cytochrome C residues, preventing apoptosis. It can also prevent the formation of Apaf-1 and Caspase 9 complex by acting directly upon Apaf-1 rather than Caspase 9, as shown in nematode homologs. Overview of signal transduction pathways
Bcl-xL
Bcl-2
IKK2
Mad2
C-Fos
STAT protein
P73
Caspase-9