This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by de Groot, R Articles by Sassone-Corsi, P Search for Related Content PubMed PubMed Citation Articles by de Groot, R Articles by Sassone-Corsi, P

 Previous Article  |  Next Article 

Mol Cell Biol. 1991 January; 11(1): 192-201

Positive regulation of jun/AP-1 by E1A.

Hubrecht Laboratorium, Netherlands Institute for Developmental Biology, Utrecht.

ABSTRACT

Proteins encoded by the adenovirus E1A oncogene are capable of positive and negative transcriptional regulation of both viral and cellular genes. E1A regulatory function is commonly thought to involve modifications of specific cellular factors that interact with responsive promoters. In this report we present evidence that E1A induces the activity of the jun/AP-1 transcription factor in three different cell types: P19, JEG-3, and HeLa. AP-1 binds to 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive elements (TREs); therefore, E1A might modulate a specific signal transduction pathway normally induced by activation of the protein kinase C. Binding of jun/AP-1 to a TRE is induced in all cell types studied when E1A is expressed. We observe that the expression of endogenous c-jun and jun B genes is induced by E1A, which directly transactivates the promoters of c-fos, c-jun, and jun B. Similar inducibility is obtained by treatment with retinoic acid and differentiation of P19-embryonal carcinoma cells. The E1A 13S product transactivates TRE sequences and cooperates with c-jun in the transcriptional stimulation. The 12S E1A product does not activate a TRE sequence, but cotransfection with c-jun circumvents this lack of stimulation. Coexpression of c-fos and E1A 12S, however, blocks the transactivation by c-jun, suggesting an important role for fos in determining the dominance of the 12S or 13S protein.

This article has been cited by other articles:

• Ogawa, E., Elliott, W. M., Hughes, F., Eichholtz, T. J., Hogg, J. C., Hayashi, S. (2004). Latent adenoviral infection induces production of growth factors relevant to airway remodeling in COPD. Am. J. Physiol. Lung Cell. Mol. Physiol. 286: L189-L197 [Abstract] [Full Text]  
• Yang, Y., McKerlie, C., Borenstein, S. H., Lu, Z., Schito, M., Chamberlain, J. W., Buchwald, M. (2002). Transgenic Expression in Mouse Lung Reveals Distinct Biological Roles for the Adenovirus Type 5 E1A 243- and 289-Amino-Acid Proteins. J. Virol. 76: 8910-8919 [Abstract] [Full Text]  
• Sanchez, T. A., Habib, I., Leland Booth, J., Evetts, S. M., Metcalf, J. P. (2000). Zinc Finger and Carboxyl Regions of Adenovirus E1A 13S CR3 Are Important for Transactivation of the Cytomegalovirus Major Immediate Early Promoter by Adenovirus. Am. J. Respir. Cell Mol. Bio. 23: 670-677 [Abstract] [Full Text]  
• Lee, W.-P., Liao, Y., Robinson, D., Kung, H.-J., Liu, E. T., Hung, M.-C. (1999). Axl-Gas6 Interaction Counteracts E1A-Mediated Cell Growth Suppression and Proapoptotic Activity. Mol. Cell. Biol. 19: 8075-8082 [Abstract] [Full Text]