| Literature DB >> 17157788 |
Tiziana Bruno1, Francesca De Nicola, Simona Iezzi, Daniele Lecis, Carmen D'Angelo, Monica Di Padova, Nicoletta Corbi, Leopoldo Dimiziani, Laura Zannini, Christian Jekimovs, Marco Scarsella, Alessandro Porrello, Alberto Chersi, Marco Crescenzi, Carlo Leonetti, Kum Kum Khanna, Silvia Soddu, Aristide Floridi, Claudio Passananti, Domenico Delia, Maurizio Fanciulli.
Abstract
Che-1 is a RNA polymerase II-binding protein involved in the transcription of E2F target genes and induction of cell proliferation. Here we show that Che-1 contributes to DNA damage response and that its depletion sensitizes cells to anticancer agents. The checkpoint kinases ATM/ATR and Chk2 interact with Che-1 and promote its phosphorylation and accumulation in response to DNA damage. These Che-1 modifications induce a specific recruitment of Che-1 on the TP53 and p21 promoters. Interestingly, it has a profound effect on the basal expression of p53, which is preserved following DNA damage. Notably, Che-1 contributes to the maintenance of the G2/M checkpoint induced by DNA damage. These findings identify a mechanism by which checkpoint kinases regulate responses to DNA damage.Entities:
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Year: 2006 PMID： 17157788 DOI： 10.1016/j.ccr.2006.10.012
Source DB: PubMed Journal: Cancer Cell ISSN： 1535-6108 Impact factor: 31.743