The p66shc adaptor protein controls oxidative stress response and life span in mammals

We report that targeted mutation of the mouse p66shc gene induces stress resistance and prolongs life span. p66shc is a splice variant of p52shc/p46shc, a cytoplasmic signal transducer involved in the transmission of mitogenic signals from activated receptors to Ras3

Enrica Migliaccio; Marco Giorgio; Simonetta Mele; Giuliana Pelicci; Paolo Reboldi; Pier Paolo Pandolfi; Luisa Lanfrancone; Pier Giuseppe Pelicci


Scholarcy highlights

  • Gene mutations in invertebrates have been identified that extend life span and enhance resistance to environmental stresses such as ultraviolet light or reactive oxygen species1
  • We show that: p66shc is serine phosphorylated upon treatment with hydrogen peroxide or irradiation with ultraviolet light; ablation of p66shc enhances cellular resistance to apoptosis induced by H2O2 or ultraviolet light; a serine-phosphorylation defective mutant of p66shc cannot restore the normal stress response in p66shc-/- cells; the p53 and p21 stress response is impaired in p66shc-/- cells; p66shc-/- mice have increased resistance to paraquat and a 30% increase in life span
  • E.M. is the recipient of a fellowship from FIRC

Need more features? Save interactive summary cards to your Scholarcy Library.