Title |
DNA Repair in Mammalian Cells
|
---|---|
Published in |
Cellular and Molecular Life Sciences, January 2009
|
DOI | 10.1007/s00018-009-8740-3 |
Pubmed ID | |
Authors |
B. Pardo, B. Gómez-González, A. Aguilera |
Abstract |
DNA double-strand breaks (DSBs) arise in cells from endogenous and exogenous attacks on the DNA backbone, but also as a direct consequence of replication failures. Proper repair of all these DSBs is essential for genome stability. Repair of broken chromosomes is a challenge for dividing cells that need to distribute equal genetic information to daughter cells. Consequently, eukaryotic organisms have evolved multi-potent and efficient mechanisms to repair DSBs that are primarily divided into two types of pathways: nonhomologous end joining (NHEJ) and homologous recombination (HR). Here we briefly describe how eukaryotic cells sense DSBs and trigger cell cycle arrest to allow repair, and we review the mechanisms of both NHEJ and HR pathways and the choice between them. (Part of a Multi-author Review). |
X Demographics
Geographical breakdown
Country | Count | As % |
---|---|---|
United States | 1 | 100% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 1 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Germany | 1 | <1% |
Chile | 1 | <1% |
France | 1 | <1% |
India | 1 | <1% |
Thailand | 1 | <1% |
Spain | 1 | <1% |
Japan | 1 | <1% |
United States | 1 | <1% |
Unknown | 230 | 97% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 55 | 23% |
Student > Master | 40 | 17% |
Researcher | 38 | 16% |
Student > Bachelor | 28 | 12% |
Student > Doctoral Student | 16 | 7% |
Other | 25 | 11% |
Unknown | 36 | 15% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 99 | 42% |
Agricultural and Biological Sciences | 71 | 30% |
Chemistry | 6 | 3% |
Engineering | 5 | 2% |
Medicine and Dentistry | 4 | 2% |
Other | 14 | 6% |
Unknown | 39 | 16% |