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Controlled Cell Death

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By Press Release by the Max Planck Institute • • October 5, 1998

Life without death is inconceivable. Cell death, also known as apoptosis, is vital for an organism. During the development of adult organisms, structures are properly formed which requires that cells are removed in a controlled manner. If apoptosis does not take place, the effects can be serious.

Certain forms of cancer and autoimmune diseases can be traced back to a lack of apoptosis; the death of nerve cells in certain forms of Alzheimer's disease and also possibly the damage done to the brain after a stroke are the result of too much apoptosis. This basic meaning of cell death for the survival of an organism explains why a large number of scientists are working to gain more insight into the molecular mechanism which underlie this phenomenon.

Scientists at the Max Planck Institute of Biophysical Chemistry in Göttingen have shed light upon the function of the gene which acts as a switch in the chain of the molecular process and which leads to the death of a cell (Cell, Vol. 94, September 18, 1998). This gene, Apaf1 (Apoptotic protease activating factor 1) plays a central role in programmed cell death in mammals. The scientists used mice in their studies to decipher the role of this gene. They could show that this gene is important for the embryonal development of the mouse. They were also able to better define the position of the corresponding gene products in the hierarchy of events that lead to cell death.

Apaf1, as a key component of apoptosis, could become a very attractive object for many areas of medical research, for the development of new anti-cancer strategies, the treatment of neurodegenerative diseases (Alzheimer's) and other genetic diseases, which involve a malfunction of the apoptosis pathway.

Source: Max Planck Institute Press Release: October 5, 1998

Full Source:
Cecconi, F., G. Alvarez-Bolado, B. Meyer, K. Roth and P. Gruss: Apaf1 (CED-4 Homolog) regulates programmed cell death in mammalian development.
Cell, Vol. 94: 727-737, September 18, 1998

Peter Gruss
Francesco Cecconi
Max Planck Institute for Biophysical Chemistry
Gottingen, Germany
49-551-201-1504 fax

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