Progeroid laminopathies are characterized by the abnormal processing of lamin A, the appearance of misshapen nuclei, and the accumulation and persistence of DNA damage. In the present article, I consider the contribution of defective DNA damage pathways to the pathology of progeroid laminopathies. Defects in DNA repair pathways appear to be caused by a combination of factors. These include abnormal epigenetic modifications of chromatin that are required to recruit DNA repair pathways to sites of DNA damage, abnormal recruitment of DNA excision repair proteins to sites of DNA double-strand breaks, and unrepairable ROS (reactive oxygen species)-induced DNA damage. At least two of these defective processes offer the potential for novel therapeutic approaches.
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December 2011
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Conference Article|
November 21 2011
The role of DNA damage in laminopathy progeroid syndromes
Christopher J. Hutchison
Christopher J. Hutchison
1
1School of Biological and Biomedical Sciences, Durham University, South Road, Durham DH1 3LE, U.K.
1email c.j.hutchison@durham.ac.uk
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Publisher: Portland Press Ltd
Received:
August 05 2011
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© The Authors Journal compilation © 2011 Biochemical Society
2011
Biochem Soc Trans (2011) 39 (6): 1715–1718.
Article history
Received:
August 05 2011
Citation
Christopher J. Hutchison; The role of DNA damage in laminopathy progeroid syndromes. Biochem Soc Trans 1 December 2011; 39 (6): 1715–1718. doi: https://doi.org/10.1042/BST20110700
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