<img alt="由Bcl-2家族介导的细胞凋亡图" 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;"> 图示：由Bcl-2家族介导的细胞凋亡。Bcl-2家族蛋白是以Bcl-2为代表的一组凋亡调节蛋白，能够通过不同的分子机制对线粒体介导的细胞凋亡发挥重要的调控作用。 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. |
