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

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...

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Bibliographic Details
Published inRadiation protection dosimetry Vol. 122; no. 1-4; p. 150
Main Authors Krawczyk, P M, Stap, J, van Oven, C, Hoebe, R, Aten, J A
Format Journal Article
LanguageEnglish
Published England 01.12.2006
Subjects
Animals
Chromosomes - physiology
Chromosomes - radiation effects
DNA Damage - physiology
DNA Repair - physiology
DNA Repair - radiation effects
DNA-Binding Proteins - metabolism
DNA-Binding Proteins - radiation effects
Dose-Response Relationship, Radiation
Humans
Models, Biological
Radiation Dosage
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Summary: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.
ISSN:0144-8420
DOI:10.1093/rpd/ncl479