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Journal ArticleDOI

Single-strand break repair and genetic disease

Keith W. Caldecott
- 01 Aug 2008 - 
- Vol. 9, Iss: 8, pp 619-631
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TLDR
The molecular mechanisms and organization of the DNA-repair pathways that remove single-strand breaks are reviewed and the connection between defects in these pathways and hereditary neurodegenerative disease are discussed.
Abstract
Hereditary defects in the repair of DNA damage are implicated in a variety of diseases, many of which are typified by neurological dysfunction and/or increased genetic instability and cancer. Of the different types of DNA damage that arise in cells, single-strand breaks (SSBs) are the most common, arising at a frequency of tens of thousands per cell per day from direct attack by intracellular metabolites and from spontaneous DNA decay. Here, the molecular mechanisms and organization of the DNA-repair pathways that remove SSBs are reviewed and the connection between defects in these pathways and hereditary neurodegenerative disease are discussed.

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Citations
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References
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TL;DR: In this review, the cellular roles of these enzymes are examined from a molecular point of view.
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Journal ArticleDOI

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TL;DR: It is demonstrated that one function of (ADP–ribose)n is to participate in the cellular recovery from DNA damage, and specific inhibitors of poly(ADP-ribose] polymerase prevent rejoining of DNA strand breaks caused by dimethyl sulphate and cytotoxicity is enhanced thereby.
Journal ArticleDOI

Oxidative Strand Scission of Nucleic Acids: Routes Initiated by Hydrogen Abstraction from the Sugar Moiety.

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