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Science 2 February 2007:
Vol. 315. no. 5812, p. 569
DOI: 10.1126/science.315.5812.569l
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The protein p66Shc facilitates protein-protein interactions in growth factor signaling pathways. But mutations in Shc can enhance life span in mammals. This effect appears to depend on a different function of Shc whereby it exerts oxidoreductase activity in mitochondria and generates oxygen radicals that lead to cell death. Pinton et al. (p. 659; see the Perspective by Hajnóczky and Hoek) now show that the activity of Shc in the mitochondria depends on its phosphorylation by protein kinase Cbeta and consequent binding of the prolylisomerase Pin1. This leads to a conformational change in the protein and to its accumulation in mitochondria. This signaling pathway could provide a target to help delay aging.




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