施一公：通过结构生物学理解细胞凋亡机制
Mechanisms of programmed cell death through structural biology
Yigong Shi
（Center for Structural Biology, Department of Biological Sciences & Biotechnology, School of Medicine, Tsinghua University, Beijing 100084, China）
清华大学 施一公教授
Programmed cell death, also known as apoptosis, is central to the development and homeostasis of metazoans. Dysregulation of apoptosis leads to a variety of human pathologies, including cancer, autoimmune diseases, and neurodegenerative disorders. Since the concept of apoptosis was established in 1972, research efforts have led to the identifi cation of hundreds of genes that govern the initiation, execution, and regulation of apoptosis primarily in three model species: Caenorhabditis elegans, Drosophila melanogaster, and mammals. The central pathway of apoptosis is conserved among the three species. In C. elegans, cell death is carried out by the CED-3 caspase, a cysteine protease with a substrate specifi city for aspartate. Similar to mammalian caspase-3 and -9, CED-3 is synthesized as an inactive zymogen in cells and its maturation involves autocatalytic cleavages.
Autoactivation of CED-3 strictly depends on the adaptor protein CED-4, a homolog of the mammalian protein Apaf-1. In response to cell death stimuli, CED-4 is released from an inactive complex involving an asymmetric dimer of CED-4 and the Bcl-2-like protein CED-9. The freed CED-4 dimer further oligomerizes to assemble into a CED-4 apoptosome, which recruits CED-3 zymogen and facilitates its autoactivation. In this presentation, I describe the molecular mechanisms of programmed cell death in C.elegans.
施一公：通过结构生物学理解细胞凋亡机制
施一公：通过结构生物学理解细胞凋亡机制
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