Vol. 283, Issue 3, L619-L627, September 2002
Tumor necrosis factor-
activation by adenovirus E1A 13S CR3
occurs in a cell-dependent and cell-independent manner
Traci A.
Sanchez,
J. Leland
Booth, and
Jordan P.
Metcalf
Department of Internal Medicine, Pulmonary and Critical
Care Division, University of Oklahoma Health Sciences Center; and the
Program in Molecular and Cellular Biology, Oklahoma Medical Research
Foundation, Oklahoma City, Oklahoma 73104
The adenovirus
(Ad) early gene product 13S transactivates the tumor necrosis factor
(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 conserved region 3 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, whereas in Jurkat cells it was between 576
and 242. The U-937 upstream element was dependent on a site
previously designated epsilon in cooperation with an adjacent nuclear
factor-
B-2a site. Therefore, transactivation of the TNF promoter by
Ad 13S in lymphocyte and monocyte cell types involves similar
subdomains of the E1A protein, but cell-specific TNF promoter elements.
Adenoviridae; human gene expression/regulation; Jurkat cells; transactivation; U-937 cells; virus replication; zinc finger protein; third conserved region
