Scientists at the School of Medicine and Princeton University have identified the way in which a tumor-suppressing gene works--it searches out damaged DNA, which is linked to many forms of cancer, and signals other genes to repair it.
Researchers have long known that a properly working p53 molecule halts abnormal growth of cells by stopping replication. What is new is how the gene works, which scientists determined by using an electron microscope capable of magnifying up to a million times.
"What we've found is that the p53 molecule is able to scan back and forth along the DNA molecules watching for the presence of damage," said Jack Griffith, professor at the Lineberger Comprehensive Cancer Center and co-investigator in the study. "When damage is found, p53 stops and binds very tightly."
The new knowledge will enable scientists to study how mutations in the p53 gene cause cancer and what can be done to fix the mutations. The study, conducted by Griffith, graduate student Suman Lee and Princeton University's Arnold Levine, was funded by the National Institutes of Health and the U.S. Department of Veterans Affairs.
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