Expression in T-cells of the proapoptotic protein p66SHC is controlled by promoter demethylation |
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Authors: | Pezzicoli Alfredo Ulivieri Cristina Capitani Nagaja Ventura Andrea Pelicci Piergiuseppe Baldari Cosima T |
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Institution: | Department of Evolutionary Biology, University of Siena, Via Aldo Moro 2, 53100 Siena, Italy. |
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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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Keywords: | CpG methylation Chromatin Gene expression Apoptosis Lymphocyte Shc proteins |
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