Scientists explain how 'death receptors' designed to kill our cells may make the...( It turns out that from the perspecti...)

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,'" sai
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