| PubMed ID |
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26040249 |
Publish Date |
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2015 Jun |
| Journal |
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J Cell Physiol |
Species |
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| Disease Type |
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Technology |
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| Title |
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Mechanisms and Consequences of Double-strand DNA Break Formation in Chromatin. |
| Authors |
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Cannan WJ, Pederson DS |
| Affiliation |
|
Department of Microbiology and Molecular Genetics, University of Vermont, Burlington, Vermont |
| Chromothripsis Definition |
|
Close-by breakpoints: NA
Copy number states: NA
Fragments random joining: NA |
| Abstract |
|
All organisms suffer double-strand breaks (DSBs) in their DNA as a result of exposure to ionizing radiation. DSBs can also form when replication forks encounter certain DNA lesions or repair intermediates. The processing and repair of DSBs can lead to mutations, loss of heterozygosity, and chromosome rearrangements that can lead to cell death or cancer. The most common pathway used to repair DSBs in metazoans (non-homologous DNA end joining) is more commonly mutagenic than the alternative pathway (homologous recombination mediated repair). Thus, factors that influence the choice of pathways used DSB repair can affect an individual's mutation burden and risk of cancer. This review describes radiological, chemical and biological mechanisms that generate DSBs, and discusses the impact of such variables as DSB etiology, cell type, cell cycle, and chromatin structure on the yield, distribution, and processing of DSBs. The final section will focus on nucleosome-specific mechanisms that influence DSB production, and the possible relationship between higher order chromosome coiling and chromosome shattering (chromothripsis).This article is protected by copyright. All rights reserved. |
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