<html>
<blockquote type=cite cite>Fecha: jueves 10 de Julio, 13 hs. Aula de
seminarios del LFBM<br>
<br>
Invitado: Maurizio Fanciulli<br>
<font face="verdana">Department of Therapeutic Programs Development,
Regina Elena Cancer Institute</font><br>
<font face="verdana">Rome Oncogenomic Center, Regina Elena Cancer
Institute<br>
Rome, Italy</font><br>
<font face="verdana"><br>
</font>Titulo: Che-1, a new effector of checkpoint signalling<br>
<br>
Resumen: Che-1 is a RNA polymerase II binding protein involved in
the<br>
transcriptional regulation of E2F target-genes and in cell
proliferation.<br>
Recently, it has been shown that Che-1 accumulates in cells responding
to<br>
genotoxic agents, such as Doxorubicin and ionizing radiations. The
DNA<br>
damage-activated checkpoint kinases ATM and Chk2 interact with and<br>
phosphorylate Che-1, enhancing its accumulation and stability, and<br>
promoting Che-1-mediated transcription of p53-responsive genes and of
p53<br>
itself, as evidenced by microarray analysis. This transcriptional
response<br>
is suppressed by expression of a Che-1 mutant lacking ATM and Chk2<br>
phosphorylation amino acid residues, or by depletion of Che-1 by
RNA<br>
silencing. In addition, chromatin immunoprecipitation analysis has
shown<br>
that Che-1 is released from the E2F-target genes and recruited to the
p21<br>
and p53 promoters after DNA damage. Che-1 contributes to the maintenance
of<br>
the G2/M checkpoint in response to genotoxic stresses. These
findings<br>
identify a new mechanism by which the checkpoint kinases regulate, via
the<br>
novel effector Che-1, the p53 pathway.<br>
<br>
Host: Arturo Romano<br>
<br>
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