<img alt="由Bcl-2家族介導(dǎo)的細(xì)胞凋亡圖" figure="" 7:="" regulation="" of="" apoptosis="" by="" the="" bcl-2="" family"="" border="1" height="347" data-cke-saved-src="http://www.bio1000。。ｃｏｍ/uploads/allimg/120409/1441391036-0.jpg" src="http://www.bio1000。。ｃｏｍ/uploads/allimg/120409/1441391036-0.jpg" width="600" style="vertical-align: middle; border: 0px;">

圖示：由Bcl-2家族介導(dǎo)的細(xì)胞凋亡。Bcl-2家族蛋白是以Bcl-2為代表的一組凋亡調(diào)節(jié)蛋白，能夠通過不同的分子機(jī)制對線粒體介導(dǎo)的細(xì)胞凋亡發(fā)揮重要的調(diào)控作用。

In a viable Cell, the proapoptotic Bcl-2 family members Bax, Bak, and BH3-only proteins are antagonized by antiapoptotic members such as Bcl-2. In response to an apoptotic stimulus, BH3-only members are activated by transcriptional upregulation (Bax, Noxa, Puma), subcellular relocalization (Bim, Bmf), dephosphorylation (Bad), or proteolysis (Bid). Activated BH3-only proteins prevent antiapoptotic Bcl-2 members from inhibiting proapoptotic members. In addition, they might directly induce a conformational change of Bax and Bak which subsequentlyoligomerize and insert into the mitochondrial membrane where they form pores either by themselves or by associating with the permeability transition pore complex. In consequence, proapoptotic factors are released from the inner mitochondrial membrane into the cytosol, such as cytochrome c which contributes to the formation of the apoptosome and the subsequent activation of the caspase cascade.