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Licensed Unlicensed Requires Authentication Published by De Gruyter November 2, 2006

Regulatory effects of the mitochondrial energetic status on mitochondrial p66Shc

Francesca Orsini, Maurizio Moroni, Cristina Contursi, Masato Yano, PierGiuseppe Pelicci, Marco Giorgio and Enrica Migliaccio
From the journal

Abstract

p66Shc promotes apoptosis and controls the intracellular redox balance. A fraction of p66Shc exists within mitochondria, where it oxidizes cytochrome c to form hydrogen peroxide, which in turn induces mitochondrial permeability and apoptosis. However, cells tolerate p66Shc expression and accumulate oxidative damage under normal conditions, implying that the p66Shc functions must be tightly regulated. Here we review available knowledge on the regulation of p66Shc transcription, protein stabilization and post-translational modifications. In addition, we report novel investigations into the role of the mitochondrial import machinery on p66Shc activation, which highlight the energetic status of mitochondria as a crucial determinant of p66Shc function.

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Corresponding author
Corresponding author

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Published Online: 2006-11-02
Published in Print: 2006-10-01

©2006 by Walter de Gruyter Berlin New York