Skip Navigation

This Article
Right arrow Print PDF (1536K)
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 arrow Search for citing articles in:
ISI Web of Science (34)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Buschhausen, G.
Right arrow Articles by Graessmann, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Buschhausen, G.
Right arrow Articles by Graessmann, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1985, Vol. 13, No. 15 5503-5513
© 1985


Articles

Inhibition of herpes simplex thymidine kinase gene expression by DNA methylation is an indirect effect

Gregor Buschhausen, Monika Graessmann and Adolf Graessmann

Institut für Molekularbiologie und Biochemie, Freie Universität Berlin Amimallee 22, D-1000 Berlin 33, FRG

Received May 14, 1985. Accepted July 12, 1985.

The biological activity of in vitro methylated H5V-TK DNA was analysed after microinjection into thymidine kinase negative rat 2 cells. It was found that the fully methylated DNA (Hpa II methylase) was as active as the non methylated control DNA for about 48 hours after injection. DNA reextraction experiments and blot analysis showed that DNA demethylation was not the reason for the observed TK activity. With prolonged cultivation time the methylated DNA becomes rapidly inactive and 100 hrs after injection thymidine incorporation was no longer detectable in the recipient cells. In transformed cells, obtained after coinjection with SV40 DNA, the HSV-DNA was partially demethylated and inactive. Addition of 5-azacytidine to the culture medium induced further demethylation and reactivation of the thymidine kinase gene.


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
Hum Mol GenetHome page
B. Hendrich and W. Bickmore
Human diseases with underlying defects in chromatin structure and modification
Hum. Mol. Genet., October 1, 2001; 10(20): 2233 - 2242.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
F. J. Campoy, R. R. Meehan, S. McKay, J. Nixon, and A. Bird
Binding of Histone H1 to DNA Is Indifferent to Methylation at CpG Sequences
J. Biol. Chem., November 3, 1995; 270(44): 26473 - 26481.
[Abstract] [Full Text] [PDF]


Home page
Genes Dev.Home page
M Holler, G Westin, J Jiricny, and W Schaffner
Sp1 transcription factor binds DNA and activates transcription even when the binding site is CpG methylated.
Genes & Dev., September 1, 1988; 2(9): 1127 - 1135.
[Abstract] [PDF]


Home page
Genes Dev.Home page
F Watt and P L Molloy
Cytosine methylation prevents binding to DNA of a HeLa cell transcription factor required for optimal expression of the adenovirus major late promoter.
Genes & Dev., September 1, 1988; 2(9): 1136 - 1143.
[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.