Phospholipid Metabolism in Apoptosis

• Συγγραφή απο Οργανισμό/Αρχή: SpringerLink (Online service)
• Άλλοι συγγραφείς: Quinn, Peter J. (Επιμελητής έκδοσης), Kagan, Valerian E. (Επιμελητής έκδοσης)
• Μορφή: Ηλεκτρονική πηγή Ηλ. βιβλίο
• Γλώσσα: English
• Έκδοση: Boston, MA : Springer US, 2002.
• Σειρά: Subcellular Biochemistry, 36
• Θέματα: Life sciences.; Human genetics.; Human anatomy.; Biochemistry.; Life Sciences.; Biochemistry, general.; Anatomy.; Human Genetics.

 The last few years have witnessed an explosion of both interest and knowledge about apoptosis, the process by which a cell actively commits suicide. The number of publications on the topic has increased from nothing in the early 1980s to more than 10,000 papers annually today. It is now well recognized that apoptosis is essential in many aspects of normal development and is required for maintaining tissue homeostasis. The idea that life requires death seems somewhat paradoxical, but cell suicide is essential for an animal to survive. For example, without selective destruction of “non-self” T cells, an animal would lack immunity. Similarly, meaningful neural connections in the brain are whittled from a mass of cells. Further, developmental cell remodeling during tissue maturation involves programmed cell death as the major mechanism for functional and structural safe transition of undifferentiated cells to more specialized counterparts. Apoptosis research, with roots in biochemistry, developmental and cell biology, genetics, and immunology, embraces this long-ignored natural law. Failure to properly regulate apoptosis can have catastrophic consequences. Cancer and many diseases (AIDS, Alzheimer’s disease, Parkinson’s disease, heart attack, stroke, etc. ) are thought to arise from deregulation of apoptosis. As apoptosis emerges as a key biological regulatory mechanism, it has become harder and harder to keep up with new developments in this field. 

 Lipid Metabolism and Release of Cytochrome c from Mitochondria -- Interaction Between Cytochrome c and Oxidized Mitochondrial Lipids -- Plasma Membrane Phospholipid Asymmetry -- Apoptosis by Phosphatidylserine in Mammalian Cells -- Phosphatidylserine Peroxidation During Apoptosis -- Role of Nitric Oxide and Membrane Phospholipid Polyunsaturation in Oxidative Cell Death -- Oxidized LDL-Induced Apoptosis -- Induction of Apoptosis by Redox-Cycling Quinones -- Apoptosis Induced by Ionizing Radiation -- Ceramidases in the Regulation of Ceramide Levels and Function -- Effect of Ceramides on Phospholipid Biosynthesis and Its Implication for Apoptosis -- Acid Sphingomyelinase-derived Ceramide Signaling in Apoptosis -- Cellular Signaling by Sphingosine and Sphingosine 1-Phosphate -- Ceramide in Regulation of Apoptosis -- Lipid Signaling in CD95-mediated Apoptosis -- Phosphatidylinositol 3-kinase, Phosphoinositides and Apoptosis.