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Scientists explain how 'death receptors' designed to kill our cells may make them stronger
June 02, 2009
A review article published in the FASEB Journal shows that death receptors may be prime therapeutic targets for treating a wide variety of cancers, immune disorders and tissue injuries It turns out that from the perspective of cell biology, Nietzsche may have been right after all: that which does not kill us does make us stronger. In a review article published in the June 2009 print issue of The FASEB Journal ( http://www.fasebj.org), scientists from the Mayo Clinic explain how cell receptors (called "death receptors") used by the body to shut down old, diseased, or otherwise unwanted cells (called "apoptosis") may also be used to make cells heartier when facing a wide range of illnesses, from liver disease to cancer.
"Increasing our knowledge of how death receptors function will allow us to develop better and more effective therapies for several human diseases," said Gregory J. Gores, M.D., Chair of the Division of Gastroenterology and Hepatology at the Mayo Clinic in Rochester, Minn., and one of the scientists involved in the work.
In their article, Gores and his colleague, Maria Guicciardi, also from the Mayo Clinic, described the various molecular pathways activated by death receptors and the proteins involved in the process. Specifically, they looked at how these proteins interact with each other and how they redistribute within a cell. Death receptors are an essential tool for the immune system to eliminate cells that have been overtaken by viruses, undergone potentially harmful genetic modifications, or have become too old to function properly. Understanding the exact sequence of events that occurs after death receptors are activated, including identifying key proteins involved in the processes, may allow researchers to develop entirely new therapeutics. These therapeutics not only would give doctors the ability to choose when and if certain cells are taken out of service, but they would also give doctors the ability to trigger cells to shift into "survival mode."
"As far as names are concerned, nothing in biology sounds more intimidating than 'death receptors,'" said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Fortunately for us, when scientists look at the intricate machinery of how cells die, they dig up clues to longer, healthier lives."
Federation of American Societies for Experimental Biology
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Second-hand smoke-induced cardiac fibrosis is related to the fas death receptor apoptotic pathway without mitochondria-dependent pathway involvement in ... from: Environmental Health Perspectives
by Wei-Wen Kuo (Author), Chieh-Hsi Wu (Author), Shin-Da Lee (Author), James A. Lin (Author), Chia-Yih Chu (Author), Jin-Ming Hwang (Author), Kwo-Chang Ueng (Author), Mu-Hsin Chang (Author), Yu-Lan Yeh (Author), Chau-Jong Wang (Author), Jer-Yuh Liu (Author), Chih-Yang Huang (Author)
This digital document is an article from Environmental Health Perspectives, published by Thomson Gale on October 1, 2005. The length of the article is 4989 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.
Citation Details Title: Second-hand smoke-induced cardiac fibrosis is related to the fas death receptor apoptotic pathway without mitochondria-dependent pathway involvement in rats.(Research) Author: Wei-Wen Kuo Publication: Environmental Health Perspectives (Magazine/Journal) Date: October 1, 2005 Publisher: Thomson Gale Volume: 113 Issue: 10 Page: 1349(5)
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Spiraling Death
Payne Receptors (Primary Contributor)
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Death Receptors in Cancer Therapy (Cancer Drug Discovery and Development)
by Wafik S. El-Deiry (Editor)
An in depth review of our latest understanding of the molecular events that regulate cell death and those molecules that provide targets for developing agonists or antagonists to modulate death signaling for therapeutic purposes. The authors focus on the extrinsic system of death receptors, their regulation and function, and their abnormalities in cancer. Topics of particular interest include resistance to apoptosis, TRAIL signaling, death receptors in embryonic development, mechanisms of caspase activation, and death receptor mutations in cancer. Additional chapters address death signaling in melanoma, synthetic retinoids and death receptors, the role of p53 in death receptor regulation, immune suppression of cancer, and combination therapy with death ligands.
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Death Receptors and Cognate Ligands in Cancer (Results and Problems in Cell Differentiation)
by Holger Kalthoff (Editor)
Death receptors play a central role in directing apoptosis in mammalian cells. This process of active cell death is important for a number of biological processes, e.g. for the regulation of the immune system. Death receptors are cell surface receptors that transmit apoptotic signals initiated by corresponding death ligands. Many complex signaling pathways are activated and apoptosis is the final result of a complex biochemical cascade of events. Besides their role in the induction of cell death, evidence now exists that death receptors are able to activate several non-apoptotic signaling pathways which, depending on cellular context, may lead to apoptosis resistance, secretion of pro-inflammatory proteins, proliferation and invasive growth of cancer cells. This book...
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Oxidative Stress in Mitochondria Disorders of Aging: Mitochondria Control Cell Death (Biological Signals and Receptors, 1-2)
by M. Ebadi (Editor)
Neurons are particularly vulnerable to age-associated decline in mitochondrial function due to their high energy demand. Thus, several models are proposed implicating mtDNA damage and mutation, and subsequent mitochondrial dysfunction, as an underlying factor in a substantial number of human pathologies including aging, neurodegenerative and neuromuscular diseases, and ischemia-reperfusion injury. Furthermore, the results of clinical, biochemical and molecular biology studies suggest that defective mitochondria contribute to neurodegenerative diseases in humans. For example, Friedreich's ataxia exhibits mitochondrial iron overload, Huntington's disease is characterized by defects in mitochondrial oxidative phosphorylation and aconitase deficiency, Parkinson's disease is associated with a...
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Glutamate, Cell Death and Memory (Research and Perspectives in Neurosciences)
by P. Ascher (Author), Dennis W., Ph.D. Choi (Author), Y. Christen (Editor)
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Valsartan matches captopril after MI: preventing deaths. (myocardial infarction, the medical term for a heart attack).(Clinical Rounds): An article from: Family Practice News
by Mitchel L. Zoler (Author)
This digital document is an article from Family Practice News, published by International Medical News Group on December 15, 2003. The length of the article is 852 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.
Citation Details Title: Valsartan matches captopril after MI: preventing deaths. (myocardial infarction, the medical term for a heart attack).(Clinical Rounds) Author: Mitchel L. Zoler Publication: Family Practice News (Magazine/Journal) Date: December 15, 2003 Publisher: International Medical News Group Volume: 33 Issue: 24 Page: 23(1)
Distributed by Thomson...
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Life and Death in the Nervous System
by C. F. Ibanez (Editor), T. Hokfelt (Editor), L. Olson (Editor), K. Fuxe (Editor), H. Jornvall (Editor), D. Ottoson (Editor)
Hardbound. In multicellular organisms, survival, proliferation and differentiation of a given cell depend upon signals produced by other cells, resulting in the coordinated development and function of the various tissues and organs. In the nervous system, the social control of cell survival and differentiation is achieved through the action of distinct groups of polypeptides collectively known as neurotrophic factors. Through the study of nerve growth factor (NGF), the other members of the neurotrophin family and other neurotrophic molecules, we have begun to understand the mechanisms that govern life and death in the nervous system. The collection of chapters in this book offers a comprehensive view of the state-of-the-art in one of the fastest growing fields of neuroscience. From the...
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Life and Death in the Nervous System: Role of Neurothropic Factors and Their Receptors
by C. F. Ibaanez (Author)
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