NDLI: Deregulation of Cdt1 induces chromosomal damage without rereplication and leads to chromosomal instability.

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Deregulation of Cdt1 induces chromosomal damage without rereplication and leads to chromosomal instability.

Content Provider	Semantic Scholar
Author	Tatsumi, Yasutoshi Sugimoto, Nozomi Yugawa, Takashi Narisawa-Saito, Mako Kiyono, Tohru Fujita, Masatoshi
Copyright Year	2006
Abstract	The activity of human Cdt1 is negatively regulated by multiple mechanisms. This suggests that Cdt1 deregulation may have a deleterious effect. Indeed, it has been suggested that overexpression of Cdt1 can induce rereplication in cancer cells and that rereplication activates Ataxia-telangiectasia-mutated (ATM) kinase and/or ATM- and Rad3-related (ATR) kinase-dependent checkpoint pathways. In this report, we highlight a new and interesting aspect of Cdt1 deregulation: data from several different systems all strongly indicate that unregulated Cdt1 overexpression at pathophysiological levels can induce chromosomal damage other than rereplication in non-transformed cells. The most important finding in these studies is that deregulated Cdt1 induces chromosomal damage and activation of the ATM-Chk2 DNA damage checkpoint pathway even in quiescent cells. These Cdt1 activities are negatively regulated by cyclin A/Cdks, probably through modification by phosphorylation. Furthermore, we found that deregulated Cdt1 induces chromosomal instability in normal human cells. Since Cdt1 is overexpressed in cancer cells, this would be a new molecular mechanism leading to carcinogenesis.
File Format	PDF HTM / HTML
Alternate Webpage(s)	http://jcs.biologists.org/content/joces/early/2006/07/11/jcs.03031.full.pdf
PubMed reference number	16835273v1
Volume Number	119
Part	15
Journal	Journal of cell science
Language	English
Access Restriction	Open
Subject Keyword	CDT1 Gene Carcinogenesis Cell Cycle Checkpoints Chromosomal Instability DNA Replication Factor DNA damage checkpoint Deregulation Episodic ataxia type 2 (disorder) Telangiectasis cancer cell
Content Type	Text
Resource Type	Article

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