PUMA travels from the nucleus to the cytoplasm to free p53 from the grip of Bcl-xL, allowing p53 to trigger signaling on mitochondria that leads to cell death, according to St. Jude
The discovery of how the activities of the protein p53 initiate signals that trigger cell suicide offers critical insights for developing new anti-cancer drugs, according to investigators from St. Jude Childrens Research Hospital. A report on this work appears in the September 9 issue of Science.
The new study showed that the protein PUMA frees p53 from the grip of a third protein, Bcl-xL, so p53 can activate the series of signals that triggers programmed cell suicide, or apoptosis. Apoptosis is the mechanism by which abnormal cells are eliminated from the body before they can cause disease, including cancer. For example, if the cell suffers a non-repairable injury to its genetic material, the p53 gene becomes active and produces the p53 protein, which accumulates both in the nucleus and cytoplasm of the damaged cell. The accumulation of p53 in the cytoplasm and nucleus each contribute to apoptosis, but until this finding, scientists did not know these contributions were linked.
Carrie Strehlau | EurekAlert!
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