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Nucleic Acids Research, 2002, Vol. 30, No. 13 2758-2763
© 2002 Oxford University Press

Deficiency of a novel mismatch repair activity in a bladder tumor cell line

Liya Gu, Jianxin Wu, Bei-Bei Zhu and Guo-Min Li*

Department of Pathology and Laboratory Medicine, Suite MS 117, Markey Cancer Center, University of Kentucky Medical Center, Lexington, KY 40536, USA

We demonstrate here that a cell line derived from a bladder cancer is defective in strand-specific mismatch repair. The mismatch repair deficiency in this cell line is associated with microsatellite instability and blocks an early step in the repair pathway. Since the addition of a known mismatch repair component hMutS{alpha}, hMutSß, hMutL{alpha}, replication protein A or proliferating cellular nuclear antigen could not restore mismatch repair to the mutant extract, the bladder tumor cell line is likely to be defective in an uncharacterized repair component. However, the repair in the mutant extract could be complemented by a partially purified activity derived from HeLa nuclear extracts. Therefore, in addition to revealing that a loss of mismatch repair function is associated with bladder cancer, this study provides information implicating a new mismatch repair activity.

* To whom correspondence should be addressed. Tel: +1 859 257 7053; Fax: +1 859 323 2094; Email: gmli{at}uky.edu


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Y. Zhang, F. Yuan, D. Wang, L. Gu, and G.-M. Li
Identification of Regulatory Factor X as a Novel Mismatch Repair Stimulatory Factor
J. Biol. Chem., May 9, 2008; 283(19): 12730 - 12735.
[Abstract] [Full Text] [PDF]


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