| Autor: |
Cahill D; Radiation Oncology Research Laboratory, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA., Connor B, Carney JP |
| Jazyk: |
angličtina |
| Zdroj: |
Frontiers in bioscience : a journal and virtual library [Front Biosci] 2006 May 01; Vol. 11, pp. 1958-76. Date of Electronic Publication: 2006 May 01. |
| DOI: |
10.2741/1938 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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