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Cellular survival after radiation exposure depends on the specific protein behavior
Exposure to radiation can wreak indiscriminate havoc on cells, tissues, and organs. Curiously, however, some tissues are more vulnerable to radiation damage than others.
Scientists have known these differences involve the protein p53, a well-studied tumor-suppressor protein that initiates a cell s auto-destruct programs. Yet, levels of this sentinel protein are often similar in tissues with vastly different sensitivities to radiation, posing the question: How is p53 involved?
A new study by researchers in the Blavatnik Institute at Harvard Medical School, Massachusetts General Hospital, and the Novartis Institutes for BioMedical Research now sheds light on this mystery.
Reporting in
Nature Communications on Feb. 9, they describe how cellular survival after radiation exposure depends on behavior of p53 over time. In vulnerable tissues, p53 levels go up and remain high, leading to cell death. In tissues that tend to survive radiation damage, p53 levels oscillate up and down.
“Dynamics matter. How things change over time matters,” said co-corresponding author Galit Lahav, the Novartis Professor of Systems Biology at HMS. “Our ability to understand biology is limited when we only look at snapshots. By seeing how things evolve temporally, we gain much richer information that can be critical for dissecting diseases and creating new therapies.”