Skip Navigation

This Article
Right arrow Print PDF (2816K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Offringa, R.
Right arrow Articles by van der Eb, A.J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Offringa, R.
Right arrow Articles by van der Eb, A.J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1988, Vol. 16, No. 23 10973-10984
© 1988

MOLECULAR BIOLOGY

Similar effects of adenovirus E1A and glucocorticoid hormones on the expression of the metalloprotease stromelysin

R. Offringa, A.M.M. Smits, A. Houweling, J.L. Bos and A.J. van der Eb

Laboratory for Molecular Carcinogenesis, Sylvius Laboratories P0 Box 9503, 2300 RA Leiden, The Netherlands

Received September 29, 1988. Accepted November 4, 1988.

The stromelysin (sml) gene encodes a secreted protease which degrades components of the extracellular matrix. Transformation of NRK49F cells by the E1A region of adenovirus (Ad) type 5 or 12 reduces sml RNA levels, whereas various growth factors or EJras-mediated transformation stimulate sml gene expression in these cells. Nuclear run-on experiments show that AdE1A, growth factors and EJras act on sml gene expression at the level of transcription. Although the sml gene is strongly suppressed in AdE1A-transformed cells, treatment with growth factors or transfection of EJras still causes a raise in sml mRNA levels, indicating that E1A does not block the induction mechanism itself. The effect of glucocorticoid hormones on sml gene expression is very similar to that of AdE1A in that mRNA levels are lowered without affecting the induction phenomenon. This similarity may provide a clue to the mechanist by which AdE1A represses cellular gene activity.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
E. Ogawa, W. M. Elliott, F. Hughes, T. J. Eichholtz, J. C. Hogg, and S. Hayashi
Latent adenoviral infection induces production of growth factors relevant to airway remodeling in COPD
Am J Physiol Lung Cell Mol Physiol, January 1, 2004; 286(1): L189 - L197.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
W.-P. Lee, Y. Liao, D. Robinson, H.-J. Kung, E. T. Liu, and M.-C. Hung
Axl-Gas6 Interaction Counteracts E1A-Mediated Cell Growth Suppression and Proapoptotic Activity
Mol. Cell. Biol., December 1, 1999; 19(12): 8075 - 8082.
[Abstract] [Full Text] [PDF]

Home page
 Genes Dev.Home page
T Braun, E Bober, and H H Arnold
Inhibition of muscle differentiation by the adenovirus E1a protein: repression of the transcriptional activating function of the HLH protein Myf-5.
Genes & Dev., May 1, 1992; 6(5): 888 - 902.
[Abstract] [PDF]

Home page
 Genes Dev.Home page
C Rochette-Egly, C Fromental, and P Chambon
General repression of enhanson activity by the adenovirus-2 E1A proteins.
Genes & Dev., January 1, 1990; 4(1): 137 - 150.
[Abstract] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.