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Radiation Protection Dosimetry Advance Access originally published online on January 17, 2007
Radiation Protection Dosimetry 2006 122(1-4):150-153; doi:10.1093/rpd/ncl479
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© The Author 2006. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Clustering of double strand break-containing chromosome domains is not inhibited by inactivation of major repair proteins

P. M. Krawczyk{dagger}, J. Stap{dagger}, C. van Oven, R. Hoebe and J. A. Aten*

Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands

* Corresponding author: J.A.Aten{at}amc.uva.nl


  Abstract

For efficient repair of DNA double strand breaks (DSBs) cells rely on a process that involves the Mre11/Rad50/Nbs1 complex, which may help to protect non-repaired DNA ends from separating until they can be rejoined by DNA repair proteins. It has been observed that as a secondary effect, this process can lead to unintended clustering of multiple, initially separate, DSB-containing chromosome domains. This work demonstrates that neither inactivation of the major repair proteins XRCC3 and the DNA-dependent protein kinase (DNA-PK) nor inhibition of DNA-PK by vanillin influences the aggregation of DSB-containing chromosome domains.


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