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Cell biology

p53 triggers cell death in stroke

Nature volume 486, pages 442443 (28 June 2012) | Download Citation

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The protein p53 is known to suppress tumour growth, which it does in part by initiating apoptosis, or programmed cell death. However, p53 also triggers another form of cell death — necrosis — that occurs in conditions such as stroke.

Ute Moll at Stony Brook University in New York and her team studied the effects of adding purified p53 to mitochondria — the cell's power-generating organelles — isolated from mouse cells. The authors found that p53 causes certain pores in the mitochondrial membrane to open up by interacting with a protein, cyclophilin D, that regulates the pore. Treating cells with an oxidizing chemical kicks off this process, which ultimately leads to necrosis.

The researchers detected the two-protein complex in injured brain tissue from mice in which a cerebral artery had been temporarily blocked as a model of stroke. Preventing complex formation protected against stroke-induced injury.

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https://doi.org/10.1038/486442d

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