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The genome guardian's dimmer switch: Regulating p53 is a matter of life or death
Date:6/30/2011

LA JOLLA, CA Scientists at the Salk Institute for Biological Studies have found clues to the functioning of an important damage response protein in cells. The protein, p53, can cause cells to stop dividing or even to commit suicide when they show signs of DNA damage, and it is responsible for much of the tissue destruction that follows exposure to ionizing radiation or DNA-damaging drugs such as the ones commonly used for cancer therapy. The new finding shows that a short segment on p53 is needed to fine-tune the protein's activity in blood-forming stem cells and their progeny after they incur DNA damage.

"It's like a dimmer switch, or rheostat, that helps control the level of p53 activity in a critical stem cell population and the offspring they generate," says Geoffrey M. Wahl, professor in the Salk Institute's Gene Expression Laboratory, and senior author of the study, which appears online in the journal Genes & Development on July 1, 2011. "In principle, controlling this switch with drugs could reduce the unwanted effects from DNA-damaging chemotherapy or radiation treatment, allowing higher doses to be used."

The protein p53 is an important tumor suppressor because it can destroy or halt the growth of cells that develop potential cancer-causing DNA mutations. But as Wahl's lab and others have shown over the past several years, p53 has much broader importance in the life and death of cells. "It's critical for determining whether a cell survives stress and continues to function in a variety of situations," says Wahl.

One problem with p53 is that it apparently evolved to protect the integrity of the genome for future generations, rather than to prolong the lives of individual cells or animals. From the point of view of an animal, p53 sometimes goes too far in killing cells or suppressing growth. Experiments in mice have suggested that even modest reductions in p53's activity greatly increases survival after exposure to rad
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Contact: Andy Hoang
ahoang@salk.edu
619-861-5811
Salk Institute
Source:Eurekalert

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