Skip Navigation

This Article
Right arrow Print PDF (2061K)
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 Tsukiyama, T.
Right arrow Articles by Niwa, O.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tsukiyama, T.
Right arrow Articles by Niwa, O.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1992, Vol. 20, No. 7 1477-1482
© 1992


MOLECULAR BIOLOGY

Isolation of high affinity cellular targets of the embryonal LTR binding protein, an undifferentiated embryonal carcinoma cell-specific repressor of Moloney leukemia virus

Toshio Tsukiyama and Ohtsura Niwa

Department of Pathology, Research Institute for Nuclear Medicine and Biology, Hiroshima University 1–2–3 Kasumi, Minami-ku, Hiroshima 734, Japan

Received February 17, 1992. Revised March 16, 1992. Accepted March 16, 1992.

ELP, the embryonal LTR binding protein, is a member of the nuclear receptor superfamily and a mouse homologue of Drosophlla FTZ-F1. ELP is expressed specifically in undifferentiated mouse embryonal carcinoma cells and participates in suppression of the Moloney murine leukemia virus genome. The zinc finger domain of the protein was fused with glutathione S-transferase and was successfully used for isolating genomic targets. Sixteen genomic fragments were isolated and twelve of them strongly interacted with ELP. Six of the ELP binding fragments were analyzed further. All of these contained the multiple binding sites for ELP, which matched well with the consensus binding sequence for FTZ-F1, YCAAGGYCR. Among these, three fragments functioned as negative regulatory elements in response to ELP, when placed upstream to the promoter region of the Moloney leukemia virus. These results indicate that ELP may function as a negative transcription factor for a variety of cellular sequences, in addition to suppressing expression of Moloney leukemia virus in early embryonal cells. It was also shown that the procedure employed here works well for isolation of genomic targets of transcription factors.


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
J. Biol. Chem.Home page
E. Barnea and Y. Bergman
Synergy of SF1 and RAR in Activation of Oct-3/4 Promoter
J. Biol. Chem., February 25, 2000; 275(9): 6608 - 6619.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
N. Sugiura, T. Suga, Y. Ozeki, G. Mamiya, and K. Takishima
The Mouse Extracellular Signal-regulated Kinase 2 Gene. GENE STRUCTURE AND CHARACTERIZATION OF THE PROMOTER
J. Biol. Chem., August 22, 1997; 272(34): 21575 - 21581.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
N. Yang, H. Shigeta, H. Shi, and C. T. Teng
Estrogen-related Receptor, hERR1, Modulates Estrogen Receptor-mediated Response of Human Lactoferrin Gene Promoter
J. Biol. Chem., March 8, 1996; 271(10): 5795 - 5804.
[Abstract] [Full Text] [PDF]


Home page
J. Biol. Chem.Home page
M. Ito, J. C. Achermann, and J. L. Jameson
A Naturally Occurring Steroidogenic Factor-1 Mutation Exhibits Differential Binding and Activation of Target Genes
J. Biol. Chem., October 6, 2000; 275(41): 31708 - 31714.
[Abstract] [Full Text] [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.