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Nucleic Acids Research 2005 33(8):2475-2485; doi:10.1093/nar/gki542
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Published online 29 April 2005

© The Author 2005. Published by Oxford University Press. All rights reserved
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions{at}oupjournals.org

Article

Repair of cyclobutane pyrimidine dimers or dimethylsulfate damage in DNA is identical in normal or telomerase-immortalized human skin fibroblasts

Steven E. Bates, Ning Ye Zhou, Laura E. Federico, Liqun Xia and Timothy R. O'Connor*

Department of Biology, Beckman Research Institute, City of Hope National Medical Center 1450 East Duarte Road, Duarte, CA 91010, USA

*To whom correspondence should be addressed. Tel: +1 626 301 8220; Fax: +1 626 930 5366; Email: toconnor{at}coh.org

Received February 12, 2005. Revised April 12, 2005. Accepted April 12, 2005.

The progression of a normal cell to senescence in vivo and in vitro is accompanied by a reduction in the length of the telomeres, the chromosome capping segments at the end of each linkage group. However, overexpression of the reverse transcriptase subunit (HTERT) of the ribonucleoprotein telomerase restores telomere length and delays cellular senescence. Although some data exist in the literature with respect to survival, no molecular data have shown that DNA repair in telomerase-immortalized cells is normal. Several telomerase-immortalized human skin fibroblast cell lines were constructed from a primary human fibroblast cell line. The primary line and the telomerase-immortalized cell lines were treated with either ultraviolet (UV) radiation or dimethylsulfate (DMS). UV radiation principally produces cyclobutane pyrimidine dimers that are repaired by nucleotide excision repair, whereas DMS introduces mainly N-methylpurines repaired by base excision repair. Here, we show that repair of both types of damage in the telomerase-immortalized human skin fibroblast cell lines is identical to repair observed in normal skin fibroblasts. Thus, telomerase expression and consequent immortalization of skin fibroblasts do not alter nucleotide or base excision repair in human cells.


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D. J. Baker, G. Wuenschell, L. Xia, J. Termini, S. E. Bates, A. D. Riggs, and T. R. O'Connor
Nucleotide Excision Repair Eliminates Unique DNA-Protein Cross-links from Mammalian Cells
J. Biol. Chem., August 3, 2007; 282(31): 22592 - 22604.
[Abstract] [Full Text] [PDF]


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