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

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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Pezzicoli A,Ulivieri C,Capitani N,Ventura A,Pelicci P,Baldari CT

doi

10.1016/j.bbrc.2006.08.039

subject

Has Abstract

pub_date

2006-10-13 00:00:00

pages

322-8

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(06)01844-4

journal_volume

349

pub_type

杂志文章

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