Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1939087 | Biochemical and Biophysical Research Communications | 2006 | 7 Pages |
Abstract
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.
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Authors
Alfredo Pezzicoli, Cristina Ulivieri, Nagaja Capitani, Andrea Ventura, Piergiuseppe Pelicci, Cosima T. Baldari,