Expression in T-cells of the proapoptotic protein p66SHC is controlled by promoter demethylation

Alfredo Pezzicoli, Cristina Ulivieri, Nagaja Capitani, Andrea Ventura, Piergiuseppe Pelicci, Cosima T. Baldari

Research output: Contribution to journalArticlepeer-review


p66Shc plays a key role in oxidative stress-induced apoptosis. p66Shc gene expression is tissue-specific and controlled by promoter methylation. In T-cells p66Shc expression is induced by a variety of apoptotic stimuli. We have addressed the mechanisms regulating p66Shc expression in T-cells. We show that the increase in p66Shc protein following stimulation with a Ca2+ ionophore results from enhanced gene expression, which is primarily dependent on DNA replication-independent promoter demethylation. Our data underline the role of CpG methylation in the control of p66Shc gene expression and provide evidence that Ca2+ signaling may lead to epigenetic modifications in nondividing cells.

Original languageEnglish
Pages (from-to)322-328
Number of pages7
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - Oct 13 2006


  • Apoptosis
  • Chromatin
  • CpG methylation
  • Gene expression
  • Lymphocyte
  • Shc proteins

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology


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