Apoptosis, or programmed cell death, is a necessary process by which a cell may die without adversely affecting its environment. It plays a crucial role in normal development, and in the body's defence mechanisms against disease. Too much cell death is destructive, leading to neurodegenerative diseases and impaired development. Conversely, too little cell death can lead to an increased susceptibility to cancer and sustained viral infection. Apoptosis is a matter of balance
Dramatic progress has been made in the study of apoptosis over the past decade. One of the most rapidly expanding knowledge bases being established is on the molecular mechanisms controlled by a variety of gene products including Bcl-2, caspases, death receptors, and proteolytic targets, as well as the central role of the mitochondrion. The major challenge in apoptosis research is how the protein products involved operate in an intricate web of signaling pathways that also play a crucial role in cell proliferation and differentiation. This book concentrates on elucidating these signal transduction mechanisms, an area not properly reviewed by other apoptosis texts.
Table of Contents
1. The Role of Sphigolipids in Stress Responses and Apoptosis in Eukaryotes 2. Radiation Response Pathways and Apoptosis 3. Apoptosis in Drosophila 4. Baculoviral Lessons in Apoptosis 5. The Mitochondrion: Decisive for Cell Death Control? 6. Caspases and the Commitment to Death 7. Killer Cells - Deliverers of Exogenous Death Proteases 8. Protein Kinase C Isoenzymes: Evidence for Selectivity in the Regulation of Apoptosis 9, The Death Receptors 10. Kinase Cascades and Apoptosis 11. Caspases: The Molecular Effectors of Apoptosis 12.
Substrates of Cell Death Proteases and Their Role in Apoptosis