English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

p66 Shc  promotes apoptosis and controls the intracellular redox balance. A fraction of p66 Shc  exists within mitochondria, where it oxidizes cytochrome  c  to form hydrogen peroxide, which in turn induces mitochondrial permeability and apoptosis. However, cells tolerate p66 Shc  expression and accumulate oxidative damage under normal conditions, implying that the p66 Shc  functions must be tightly regulated. Here we review available knowledge on the regulation of p66 Shc  transcription, protein stabilization and post-translational modifications. In addition, we report novel investigations into the role of the mitochondrial import machinery on p66 Shc  activation, which highlight the energetic status of mitochondria as a crucial determinant of p66 Shc  function.

Regulatory effects of the mitochondrial energetic status on mitochondrial p66 Shc