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UT MD Anderson discovery wins 2010 Cozzarelli Prize
Date:2/23/2011

alth Science Center at Houston (UTHealth).

"The initial discovery by postdoctoral fellow Shengli Cai, Ph.D., Angela's first authorship and excellent collaboration with scientists at other institutions all made this a great project," Walker said.

The team discovered that ATM (short for Ataxia-Telangiectasia Mutated) recognizes damage caused by reactive oxygen species (ROS) in the cytoplasm and tells the cell to stop growing or orders the cell to consume itself, a process called autophagy.

Reactive oxygen species are a byproduct of cellular metabolism. They react with other molecules, are toxic in large amounts and kept in check by antioxidants. When that balance is disrupted, elevated ROS levels damage proteins, lipids and DNA.

Elevated ROS has been linked to more than 150 diseases, including diabetes, cancer, neurodegenerative diseases and atherosclerosis.

In its previously known role, ATM notices DNA damage, orders the cell to repair the damage and halts cell division. If repair is not possible, ATM sets off apoptosis - programmed cell death. ATM is commonly mutated in cancer.

ATM sets off a molecular chain of events to kill ROS-damaged cells that includes the tumor-suppressor TSC2, the protein originally targeted by the researchers.

One possibility raised by this research, Walker said, is the ability to activate ATM without damaging DNA.


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Contact: Scott Merville
smerville@mdanderson.org
713-792-0667
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert  

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