Skip Navigation



Mutagenesis Advance Access published online on June 14, 2006
Mutagenesis, doi:10.1093/mutage/gel024
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow Supplementary data
Right arrow All Versions of this Article:
21/4/219    most recent
gel024v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by El-Khamisy, S. F.
Right arrow Articles by Caldecott, K. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by El-Khamisy, S. F.
Right arrow Articles by Caldecott, K. W.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please email: journals.permissions@oxfordjournals.org
Received April 11, 2006
Revised May 8, 2006
Accepted May 8, 2006

Review

TDP1-dependent DNA single-strand break repair and neurodegeneration

Sherif F. El-Khamisy 1 * and Keith W. Caldecott 2

1 Biochemistry Department, Faculty of Pharmacy, Ain Shams University, PO Box 11566, Cairo, Egypt
2 Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, UK

* To whom correspondence should be addressed.
Sherif F. El-Khamisy, E-mail: smfame20{at}sussex.ac.uk


  Abstract

DNA single-strand breaks (SSBs) are the commonest DNA lesions that arise spontaneously in living cells. Cells employ efficient processes for the rapid repair of these breaks and defects in these processes appear to preferentially impact on the nervous system, causing human ataxia. Spinocerebellar ataxia with axonal neuropathy (SCAN1) is a human disease that is associated with a defect in repairing certain types of SSBs. Although it is a rare neurodegenerative disease, understanding the molecular basis of SCAN1 will lead to better understanding of the mechanisms that underpin not only neurodegeneration but also cancer.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Nucleic Acids ResHome page
A. Kulkarni, D. R. McNeill, M. Gleichmann, M. P. Mattson, and D. M. Wilson III
XRCC1 protects against the lethality of induced oxidative DNA damage in nondividing neural cells
Nucleic Acids Res., September 1, 2008; 36(15): 5111 - 5121.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.