Abstract
The protein p66 Shc 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 . now show that the activity of Shc in the mitochondria depends on its phosphorylation by protein kinase C β and consequent binding of the prolyl isomerase 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. P. Pinton, A. Rimessi, S. Marchi, F. Orsini, E. Migliaccio, M. Giorgio, C. Contursi, S. Minucci, F. Mantovani, M. R. Wieckowski, G. Del Sal, P. G. Pelicci, R. Rizzuto, Protein kinase C β and prolyl isomerase 1 regulate mitochondrial effects of the life-span determinant p66 Shc . Science 315 , 659-663 (2007). [Abstract] [Full Text] G. Hajnóczky, J. B. Hoek, Mitochondrial longevity pathways. Science 315 , 607-609 (2007). [Summary] [Full Text]
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
