本课题用蛋白晶体X衍射及相关定点突变和一系列生化方法对Apaf-1是如何组装成为凋亡复合体以及凋亡复合体是如何结合并激活Caspase-9的分子机理进行研究，阐明细胞色素C介导的内源性细胞调亡起始环节的分子机理，建立和完善Caspase-9的激活的分子调节机制模型,为研究人类癌症、自免疫疾病及神经退行性疾病等重大疾病的致病机理,研究开发治愈这些疾病的新型药物提供重要的理论依据。

Apoptosis is a fundamental and crucial process for higher animals. A detailed molecular mechanism of apoptosome formation and apoptosis initiation is extremly important to answering the formation of human cancer, autoimmunity disease, and neurodegenerative disease. Based on the results of these research it is very likely to give a theoretical guidence to the drug design for these disease. By employing X-ray crystallography, site-directed mutagenesis and other biochemical analysis, this project is carrying out an important exploration for the molecular mechanism of how Caspase-9 is activated through Apoptosome.This research will demonstrate how intrinsic apoptosis is initiated by the releasing of cytochrome C, build up and complete a reasonable model of Caspase-9 activation.