Includes bibliographical references and index.
|Statement||organized and edited by G.C. Brown, D.G. Nicholls and C.E. Cooper.|
|Series||Biochemical Society symposium -- no. 66.|
|Contributions||Brown, Guy C., Nicholls, David G., Cooper, Chris E.|
|The Physical Object|
|Pagination||x, 225 p. :|
|Number of Pages||225|
Mitochondria and Cell Death, part of the Cell Death in Biology and Diseases series, is invaluable reading for graduate students, researchers, and clinicians in the fields of neuroscience, oncology, gastroenterology, and hepatology, as well as those interested . Get this from a library! Mitochondria and cell death. [Guy C Brown; David G Nicholls; Chris E Cooper;] -- "This book reviews the role of mitochondria in cell death and disease through a series of chapters which present the latest research and thinking on the subject from some of the key researchers in. Mitochondria and Cell Death, part of the Cell Death in Biology and Diseases series, is invaluable reading for graduate students, researchers, and clinicians in the fields of neuroscience, oncology, gastroenterology, and hepatology, as well as those interested Format: Hardcover. Mitochondria integrate a host of pro- and antiapoptotic and necrotic signaling pathways, and are the initial domino in several cell death cascades. 13,42 Indeed, mitochondrial dysfunction is rapidly becoming appreciated as an important etiological component in a wide variety of both acute and chronic human diseases, 43–45 as well as in.
This book includes chapters covering the involvement of mitochondria in Parkinson's disease, encephalopathies, tumorigenesis, muscular dystrophy, and other diseases, as well as aging. It is thus a vital reference for all cell and molecular biologists, as well as researchers working on muscle and neurodegenerative diseases, the role of 5/5(1). Although required for life, paradoxically, mitochondria are often essential for initiating apoptotic cell death. Mitochondria regulate caspase activation and cell death through an event termed mitochondrial outer membrane permeabilization (MOMP); this leads to the release of various mitochondrial intermembrane space proteins that activate caspases, resulting in by: Introduction. Mitochondria are integral to normal cellular function as they are responsible for energy production in eukaryotes, including the synthesis of phospholipids and heme, calcium homeostasis, apoptotic activation and cell death. 1,2 Alterations in mitochondrial function often associate with disease states including endocrine related disorders such as diabetes mellitus, reflecting the Cited by: Mitochondria and Cell Death. Annual Plant Reviews book series, Volume Plant Mitochondria, 2nd Edition. Olivier Van Aken. ARC Centre of Excellence in Plant Energy Biology, University of Western Australia, Crawley, Australia. Department of Biology, Lund University, 35 Sölvegatan, Lund, : Olivier Van Aken, Olivier Van Aken.
The mitochondrion has long been known both as a chemical powerplant and as a cellular compartment housing various biosynthetic pathways. However, studies on the function of mitochondria in apoptotic cell death have revealed a versatility and complexity of these organelles previously unsuspected. The mechanisms proposed for mitochondrial involvement in cell death are diverse and highly Cited by: Cell death, also called apoptosis, is an essential part of life. As cells become old or broken, they are cleared away and destroyed. Mitochondria help decide which cells are destroyed. The mechanism by which oocytes harboring the more defective mitochondria are recognized is unknown. However, one possibility is that the defective mitochondria generate more ROS and this leads to preferential cell death, perhaps through activation of the mtPTP (F an et al. ; S tewart et al. ).Cited by: Mitochondria and Cell Death, part of the Cell Death in Biology and Diseases series, is invaluable reading for graduate students, researchers, and clinicians in the fields of neuroscience, oncology, gastroenterology, and hepatology, as well as those interested Brand: Springer New York.