apoptosis细胞凋亡..pptVIP

IAPs (Inhibitors of apoptosis) Inhibit Caspases In the absence of an apoptotic stimulus, IAPs prevent accidental apoptosis caused by the spontaneous activation of procaspases. The IAPs are located in the cytosol and bind to ？ and inhibit any spontaneously activated caspases. Some IAPs are also ubiquitin ligases 泛素连接酶that ubiquitylate the caspases they bind to, marking them for degradation降解 in proteasomes. 蛋白酶体 When an apoptotic stimulus activates the intrinsic pathway, among the proteins released from the mitochondrial intermembrane space are anti-IAP proteins, which bind to and block the inhibitory activity of the IAPs. At the same time, the released cytochrome c triggers the assembly of apoptosomes, which can now activate a caspase cascade, leading to apoptosis. The role of survival factors and cell death in adjusting the number of developing nerve cells to the amount of target tissue More nerve cells are produced than can be supported by the limited amount of survival factors released by the target cells. Therefore, some cells receive an sufficient amount of survival factors to avoid apoptosis. This strategy of overproduction followed by culling ensures that all target cells are contacted by nerve cells and that the extra nerve cells are automatically eliminated. Extracellular Survival Factors Inhibit Apoptosis in Various Ways外源生存因子阻止凋亡 Three ways that extracellular survival factors can inhibit apoptosis 外源(受体介导) 凋亡途径 The extrinsic (receptor-mediated) pathway of apoptosis 内源(线粒体介导)凋亡途径 The intrinsic (mitochondria-mediated) pathway of apoptosis) Summary Death receptor and intrinsic pathways of apoptosis. Intrinsic pathway is mediated by mitochondrial and the endoplasmic reticulum pathways. Distinct initiator caspases are activated in each pathway of apoptosis (modified from ref. 94). Gupta et al. Immunity Ageing 2006 3:5 ? doi:10.1186/1742-4933-3-5 In contrast to their similar brain abnormalities, newborn mice deficient in Apaf1 or caspase-9 have distinct