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Radiat Prot Dosimetry. 2006;122(1-4):150-3. Epub 2007 Jan 17.

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

Author information

1
Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, Meibergdreef 15, 1105 AZ Amsterdam, The Netherlands.

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.

PMID:
17229782
DOI:
10.1093/rpd/ncl479
[Indexed for MEDLINE]

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