<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.</blockquote><br>
Publicaciones recientes:<br>
<br>
<br>
<font color="#0000FF"><u>- PLoS ONE.</u></font> 2007 Aug
22;2(1):e774.<br>
Utrophin up-regulation by an artificial transcription factor in
transgenic mice.<br>
<font color="#0000FF"><u>Mattei E</u></font>,
<font color="#0000FF"><u>Corbi N</u></font>, <font color="#0000FF"><u>Di
Certo MG</u></font>, <font color="#0000FF"><u>Strimpakos G</u></font>,
<font color="#0000FF"><u>Severini C</u></font>,
<font color="#0000FF"><u>Onori A</u></font>,
<font color="#0000FF"><u>Desantis A</u></font>,
<font color="#0000FF"><u>Libri V</u></font>,
<font color="#0000FF"><u>Buontempo S</u></font>,
<font color="#0000FF"><u>Floridi A</u></font>,
<font color="#0000FF"><u>Fanciulli M</u></font>,
<font color="#0000FF"><u>Baban D</u></font>,
<font color="#0000FF"><u>Davies KE</u></font>,
<font color="#0000FF"><u>Passananti C<br>
<br>
- J Biol Chem.</u></font> 2007 Jul 6;282(27):19685-91. Epub 2007 Apr
27.<br>
The prolyl isomerase Pin1 affects Che-1 stability in response to
apoptotic DNA damage.<br>
<font color="#0000FF"><u>De Nicola F</u></font>,
<font color="#0000FF"><u>Bruno T</u></font>,
<font color="#0000FF"><u>Iezzi S</u></font>, <font color="#0000FF"><u>Di
Padova M</u></font>, <font color="#0000FF"><u>Floridi A</u></font>,
<font color="#0000FF"><u>Passananti C</u></font>,
<font color="#0000FF"><u>Del Sal G</u></font>,
<font color="#0000FF"><u>Fanciulli M</u></font>.<br>
<font color="#0000FF"><u>- J Biol Chem.</u></font> 2007 May
18;282(20):15248-57. Epub 2007 Mar 2.<br>
A novel corepressor, BCoR-L1, represses transcription through an
interaction with CtBP.<br>
<font color="#0000FF"><u>Pagan JK</u></font>,
<font color="#0000FF"><u>Arnold J</u></font>,
<font color="#0000FF"><u>Hanchard KJ</u></font>,
<font color="#0000FF"><u>Kumar R</u></font>,
<font color="#0000FF"><u>Bruno T</u></font>,
<font color="#0000FF"><u>Jones MJ</u></font>,
<font color="#0000FF"><u>Richard DJ</u></font>,
<font color="#0000FF"><u>Forrest A</u></font>,
<font color="#0000FF"><u>Spurdle A</u></font>,
<font color="#0000FF"><u>Verdin E</u></font>,
<font color="#0000FF"><u>Crossley M</u></font>,
<font color="#0000FF"><u>Fanciulli M</u></font>,
<font color="#0000FF"><u>Chenevix-Trench G</u></font>,
<font color="#0000FF"><u>Young DB</u></font>,
<font color="#0000FF"><u>Khanna KK</u></font>.<br>
<font color="#0000FF"><u>- Cancer Cell.</u></font> 2006
Dec;10(6):473-86.<br>
Che-1 phosphorylation by ATM/ATR and Chk2 kinases activates p53
transcription and the G2/M checkpoint.<br>
<font color="#0000FF"><u>Bruno T</u></font>, <font color="#0000FF"><u>De
Nicola F</u></font>, <font color="#0000FF"><u>Iezzi S</u></font>,
<font color="#0000FF"><u>Lecis D</u></font>,
<font color="#0000FF"><u>D'Angelo C</u></font>,
<font color="#0000FF"><u>Di Padova M</u></font>,
<font color="#0000FF"><u>Corbi N</u></font>,
<font color="#0000FF"><u>Dimiziani L</u></font>,
<font color="#0000FF"><u>Zannini L</u></font>,
<font color="#0000FF"><u>Jekimovs C</u></font>,
<font color="#0000FF"><u>Scarsella M</u></font>,
<font color="#0000FF"><u>Porrello A</u></font>,
<font color="#0000FF"><u>Chersi A</u></font>,
<font color="#0000FF"><u>Crescenzi M</u></font>,
<font color="#0000FF"><u>Leonetti C</u></font>,
<font color="#0000FF"><u>Khanna KK</u></font>,
<font color="#0000FF"><u>Soddu S</u></font>,
<font color="#0000FF"><u>Floridi A</u></font>,
<font color="#0000FF"><u>Passananti C</u></font>,
<font color="#0000FF"><u>Delia D</u></font>,
<font color="#0000FF"><u>Fanciulli M</u></font>.<br>
<font color="#0000FF"><u>- Cancer Cell.</u></font> 2002
Nov;2(5):387-99.<br>
Che-1 affects cell growth by interfering with the recruitment of HDAC1 by
Rb.<br>
<font color="#0000FF"><u>Bruno T</u></font>, <font color="#0000FF"><u>De
Angelis R</u></font>, <font color="#0000FF"><u>De Nicola F</u></font>,
<font color="#0000FF"><u>Barbato C</u></font>,
<font color="#0000FF"><u>Di Padova M</u></font>,
<font color="#0000FF"><u>Corbi N</u></font>,
<font color="#0000FF"><u>Libri V</u></font>,
<font color="#0000FF"><u>Benassi B</u></font>,
<font color="#0000FF"><u>Mattei E</u></font>,
<font color="#0000FF"><u>Chersi A</u></font>,
<font color="#0000FF"><u>Soddu S</u></font>,
<font color="#0000FF"><u>Floridi A</u></font>,
<font color="#0000FF"><u>Passananti C</u></font>,
<font color="#0000FF"><u>Fanciulli M</u></font>.<br>
<br>
<br>
<br>
<br>
<blockquote type=cite cite>Host: Arturo Romano<br>
<br>
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