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Nucleic Acids Research Advance Access originally published online on February 17, 2009
Nucleic Acids Research 2009 37(7):2087-2095; doi:10.1093/nar/gkp065
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Nucleic Acids Research, 2009, Vol. 37, No. 7 2087-2095
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Genome Integrity, Repair and Replication

The human GINS complex associates with Cdc45 and MCM and is essential for DNA replication

Tomás Aparicio1, Emmanuelle Guillou1, Javier Coloma2, Guillermo Montoya2 and Juan Méndez1,*

1DNA Replication Group, Molecular Oncology Programme and 2Macromolecular Crystallography Group, Structural Biology and Biocomputing Programme, Spanish National Cancer Research Center (CNIO), Melchor Fernández Almagro, 3 E-28029 Madrid, Spain

*To whom correspondence should be addressed. Tel: +34 91 732 8000 (ext. 3490); Fax: +34 91 732 8033; Email: jmendez{at}cnio.es

Received December 27, 2008. Revised January 23, 2009. Accepted January 24, 2009.

The GINS complex, originally discovered in Saccharomyces cerevisiae and Xenopus laevis, binds to DNA replication origins shortly before the onset of S phase and travels with the replication forks after initiation. In this study we present a detailed characterization of the human GINS (hGINS) homolog. Using new antibodies that allow the detection of endogenous hGINS in cells and tissues, we have examined its expression, abundance, subcellular localization and association with other DNA replication proteins. Expression of hGINS is restricted to actively proliferating cells. During the S phase, hGINS becomes part of a Cdc45–MCM–GINS (CMG) complex that is assembled on chromatin. Down-regulation of hGINS destabilizes CMG, causes a G1–S arrest and slows down ongoing DNA replication, effectively blocking cell proliferation. Our data support the notion that hGINS is an essential component of the human replisome.


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