IMR Press / FBL / Volume 11 / Issue 2 / DOI: 10.2741/1938

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Mechanisms of eukaryotic DNA double strand break repair
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1 Radiation Oncology Research Laboratory, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA

Academic Editor: A-Lien Lu

Front. Biosci. (Landmark Ed) 2006, 11(2), 1958–1976;
Published: 1 May 2006
(This article belongs to the Special Issue DNA repair and genome stability)

For all cells, a DNA double strand break (DSB) is a dangerous lesion that can have profound consequences for the genome. If a DSB is encountered during mitosis, chromosomal separation may be adversely affected. Alternatively, during S phase a DSB may cause replication fork stalling or collapse. Improperly repaired DSBs can result in chromosomal rearrangements, senescence or activation of apoptotic pathways. Cells have developed sophisticated recombination pathways to metabolize and repair DSBs quickly as well as the capacity to differentiate physiologically occurring breaks from life threatening lesions. The two major pathways of recombination repair are known as non-homologous end-joining (NHEJ) and homologous recombination (HR). In this review, we will discuss the detection, response, and repair of DSBs in eukaryotes.

Double Strand-Break Repair
Damage Detection and Response
Homologous Recombination
Non-Homologous End Joining
Mre11 Complex
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