REGULATION OF APOPTOSIS BY ICH1S

程序性细胞死亡(或称细胞凋亡)对 发育、动态平衡以及包括癌症在内的许多疾病， 获得性免疫缺陷综合症和神经退行性疾病。 在基因控制下，它通过激活一种 内部或外部导致的内在自杀计划 信号。ICE/CED-3半胱氨酸蛋白酶家族自主发挥作用 死亡细胞中的效应器。NIDD-2/Ich-1，这个家族的成员，是 经鉴定可诱导组织培养细胞凋亡。我的 目前的研究表明，ICH-1在细胞凋亡过程中被激活。这个 本提案的总体目标是描述功能 ICH-1在细胞凋亡中的作用及其激活机制。特定的 目的包括：i)检查ICH-1在初级组织中的激活 培养细胞，特别是胸腺细胞和神经细胞，当它们 被诱导进行细胞凋亡；ii)表征活性形式 和体内ICH-1的中间产物；iii)建立 ICH-I与其他死亡基因的关系；IV)鉴定ICH-1 当它被激活时目标。

Programmed cell death (or apoptosis) is of central importance for the development, homeostasis, and in many diseases including cancer, acquired immunodeficiency syndrome, and neurodegenerative disorders. Under genetic control, it occurs through the activation of an intrinsic suicide program as a result of either internal or external signals. ICE/CED-3 cysteine protease family acts autonomously as effectors in dying cells. Nedd-2/Ich-1, a member of this family, was identified that can induce apoptosis in tissue culture cells. My current work suggested that ICH-1 is activated during apoptosis. The overall objective of this proposal is to characterize the functional role of ICH-1 in apoptosis,and its activation mechanism. Specific aims include: i) to examine ICH-1 activation in primary tissue culture cells, especially thymocytes and neuronal cells, when they are induced to undergo apoptosis; ii) to characterize the active form and intermediate products of ICH-1 in vivo; iii) to establish the relationship of ICH-I with other death genes; iv) to identify ICH-1 targets when it is activated.