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Journal of Virology, December 1998, p. 9637-9644, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Cell Cycle Progression in Monkey Cells Expressing Simian Virus 40 Small t Antigen from Adenovirus Vectors

Alan K. Howe,dagger Stéphanie Gaillard, John S. Bennett,Dagger and Kathleen Rundell*

Department of Microbiology-Immunology and The Lurie Cancer Center, Northwestern University, Chicago, Illinois 60611

Received 21 May 1998/Accepted 27 August 1998

The simian virus 40 small t antigen (small-t) is required for optimal viral replication and transformation, especially during the infection of nondividing cells, suggesting that the function of small-t is to promote cell cycle progression. The mechanism through which small-t promotes cell growth reflects, in part, its binding and inhibition of protein phosphatase 2A (PP2A). The use of recombinant adenoviruses allows small-t expression in a majority of cells in a population, thus providing a convenient source of cells for biochemical analyses. In monkey kidney CV1 cells, small-t expressed from these adenovirus vectors activated the mitogen-activated protein kinase (MAPK) pathway, induced JNK activity, and increased AP-1 DNA-binding activity, all in a PP2A-dependent manner. Expression of small-t also caused an increase in the phosphorylation of the Na+/H+ antiporter, a mitogen-activated ion exchanger whose activity correlates with its phosphorylation. At least part of the antiporter phosphorylation induced by small-t reflected activation of the MAPK pathway, as suggested by results of assays using a chemical inhibitor of the MAPK-activating kinase, MEK. Finally, small-t expression from adenovirus vectors promoted efficient cell cycle progression by growth-arrested cells. These vectors should facilitate further analysis of effects of small-t on cell cycle mediators.

* Corresponding author. Mailing address: Department of Microbiology-Immunology, Northwestern University, 303 E. Chicago Ave., Chicago, IL 60611. Phone: (312) 503-5923. Fax: (312) 908-1372. E-mail: krundell{at}nwu.edu.

dagger Present address: Department of Pharmacology, University of North Carolina, Chapel Hill, NC 27514.

Dagger Present address: Department of Biology, Clarke College, Dubuque, IA 52001.

Journal of Virology, December 1998, p. 9637-9644, Vol. 72, No. 12
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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