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Am J Physiol Lung Cell Mol Physiol (April 26, 2002). doi:10.1152/ajplung.00342.2001
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Articles in PresS, published online ahead of print April 26, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00342.2001
Submitted on August 27, 2001
Accepted on April 11, 2002

Tumor necrosis factor-alpha activation by Adenovirus E1A 13S CR3 occurs in a cell dependent and cell independent manner

Traci A Sanchez1, J. Leland Booth2, and Jordan P Metcalf2*

1 Pulmonary and Critical Care Division, Dept of Internal Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA
2 Pulmonary and Critical Care Division, Dept of Internal Medicine, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma, USA; Molecular and Cellular Biology, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA

* To whom correspondence should be addressed. E-mail: jordan-metcalf{at}ouhsc.edu.

The Adenovirus (Ad) early gene product 13S transactivates the tumor necrosis factor-alpha (TNF) promoter in inflammatory cells. We examined both the subdomains of E1A and the upstream TNF promoter elements involved. In both Jurkat and U-937 cells, zinc finger or carboxyl region mutation of Ad E1A 13S CR3 resulted in a significant loss of transactivation of the TNF promoter (>=69%). For both cell types there was a TNF negative regulatory element in the -242 to -199 region, and a positive regulatory element between -199 and -118. In contrast an upstream positive regulatory element was detected in different regions in both cell types. In U-937 cells the positive regulatory unit was between -600 and -576, while in Jurkat cells it was between -576 and -242. The U937 upstream element was dependent on a site previously designated Epsilon ({epsilon}) in cooperation with an adjacent NF-{kappa}B-2a site. Therefore, transactivation of the TNF promoter by adenovirus 13S in lymphocyte and monocyte cell types involves similar subdomains of the E1A protein, but cell-specific TNF promoter elements.






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