Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (71K) Freely available
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 ISI Web of Science
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 (17)
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Metcalfe, A. M.
Right arrow Articles by Radda, G. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Metcalfe, A. M.
Right arrow Articles by Radda, G. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, Vol 25, Issue 5 983-986, Copyright © 1997 by Oxford University Press

ARTICLES

Wild-type but not mutant p53 activates the hepatocyte growth factor/scatter factor promoter

AM Metcalfe, RM Dixon and GK Radda
MRC Clinical and Biochemical Magnetic Resonance Unit, Department of Biochemistry, University of Oxford, South Parks Road, Oxford OX1 3QU, UK.

p53 transactivates the expression of a variety of genes by binding to specific DNA sequences within the promoter. We have investigated the ability of wild-type p53 and a non-DNA binding p53 mutant to activate the hepatocyte growth factor/scatter factor (HGF/SF) promoter using chloramphenicol acetyltransferase reporter constructs. We also used deletion sequences of the HGF/SF promoter to identify which regions, if any, were responsible for p53 binding. Our results show that wild-type but not mutant p53 activates the HGF/SF promoter when using -3000 and - 755 bp upstream of the HGF/SF gene. This activation is lost when promoter sequences covering -365 and -239 bp are used. Analysis of the DNA sequence between -365 and -755 bp shows one putative p53 half-site with 80% homology to the consensus sequence and another half-site 3 bases downstream of this with 100% homology to the consensus sequence. In contrast to previously identified p53 binding DNA sequences, the downstream half-site is inverted. We propose that the HGF/SF promoter can be activated by wild-type p53 in vivo and that this could be as a result of a novel form of sequence-specific DNA binding.
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
 Mol. Cell. Biol.Home page
J. M. Hearnes, D. J. Mays, K. L. Schavolt, L. Tang, X. Jiang, and J. A. Pietenpol
Chromatin Immunoprecipitation-Based Screen To Identify Functional Genomic Binding Sites for Sequence-Specific Transactivators
Mol. Cell. Biol., November 15, 2005; 25(22): 10148 - 10158.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
A. A. Sablina, P. M. Chumakov, and B. P. Kopnin
Tumor Suppressor p53 and Its Homologue p73{alpha} Affect Cell Migration
J. Biol. Chem., July 18, 2003; 278(30): 27362 - 27371.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
D.-W. Seol, Q. Chen, M. L. Smith, and R. Zarnegar
Regulation of the c-met Proto-oncogene Promoter by p53
J. Biol. Chem., February 5, 1999; 274(6): 3565 - 3572.
[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.