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Cells on the verge of suicide

Rockefeller Scientist discovers molecular messengers that rescue cells from death

A developing cell in the human body sits on the edge of death. Proteins called Grim, Reaper and Hid stand poised, ready to unleash other toxic proteins. Only if a protein messenger from another cell arrives in time to call off the killing, will the cell then mature into any one of the various types of body cells, such as skin, liver and brain.

But how these protein messengers command cells to survive has remained a mystery until now. For the first time, the entire team of molecular messengers responsible for issuing certain brain cells with orders to survive has been identified by a Rockefeller University scientist and his colleagues.

They report their results in the Feb 1 issue of Developmental Cell.

"Cell death is important during development and in adulthood because it is a very stringent quality-control mechanism that makes sure there are no unwanted, potentially dangerous cells in the body," says principal investigator Hermann Steller, Ph.D., Strang Professor at Rockefeller and a Howard Hughes Medical Institute investigator.

"In fact, right now cells in our body are dying at a rate of 100,000 cells per second, while at the same time 100,000 new cells are being born."

The new research may one day lead to novel treatments for diseases in which too much or too little cell death occurs: too much cell death is associated with neurodegenerative and muscular diseases such as Alzheimer's, Parkinson's, Huntington's and stroke, while too little leads to the survival of cells with mutations, the hallmark of cancer. For example, the 55 percent of human cancers containing a mutated copy of the p53 gene no longer possess the protective ability to kill off harmful cells.

"We might be able to reinstate the mechanism of cell death in cancer cells so that they kill themselves," says Steller, who heads the Strang Laboratory of
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Contact: Whitney Clavin
clavinw@rockefeller.edu
212-327-7250
Rockefeller University
31-Jan-2002


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