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

Radiat Prot Dosimetry. 2006;122(1-4):150-3. doi: 10.1093/rpd/ncl479. Epub 2007 Jan 17.


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.

MeSH terms

  • 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


  • DNA-Binding Proteins